Behnaz Amini

Younes Demmouche

Mahmoud Barati

Guillaume Helbert

Shabnam Arbab Chirani
email: shabnam.arbab@enib.fr

Sylvain Calloch

Self-heating of metastable 304L austenitic stainless steel under cyclic loading: influence of initial martensite volume fraction, testing temperature and pre-strain

Keywords: self-heating under cyclic loading, metastable austenitic stainless steel, martensitic transformation, pre-strain

In this study, special attention is paid to the thermal response of the austenitic stainless steel 304L under cyclic loading tests (i.e., self-heating tests) in different conditions. The cyclic behavior of the 304L austenitic stainless steel can be influenced by martensitic transformation. Hence, the role of martensitic transformation in the self-heating behavior of this material is studied. For this purpose, self-heating tests are performed on pre-strained specimens at a wide range of temperatures from 100°C to -130°C, which leads to different initial volume fractions of martensite ranging from 0% to 45%, respectively. Furthermore, the influence of the testing temperature and a pre-strain at room temperature on the selfheating curves is investigated. The results demonstrate that the decrease in the test temperature from room temperature to -30°C as well as the increase in the pre-strain values from 0% to 30% at room temperature, result in a shift of the self-heating curves to the right. It could mean that the fatigue limit of the material is improved.

Introduction

Austenitic stainless steel materials have found a wide range of applications due to their interesting properties such as high ductility, good corrosion resistance, low cost, easy machining and plentiful supply. In metastable austenitic stainless steels, γ-austenite (FCC) can transform into α′-martensite (BCC) and/or ε-martensite (HCP) under the transformation-induced plasticity (TRIP) effect [START_REF] Pessoa | Influence of loading frequency and role of surface micro-defects on fatigue behavior of metastable austenitic stainless steel AISI 304[END_REF], [START_REF] Christ | Metastable Austenitic Stainless Steels and the Effect of Deformation-Induced Phase Transformation on the Fatigue Properties[END_REF]. Therefore, the mechanical properties of these materials are significantly affected by deformation-induced martensitic transformation. By applying stress or plastic deformation, 2 austenitic stainless steel can experience phase transformations through three different paths: the first two are that γ-austenite can transform directly into ε-martensite or α'-martensite, and the third is indirect transformation from γ to ε and afterwards α'-martensite [START_REF] Liu | Use of in-situ TEM to characterize the deformation-induced martensitic transformation in 304 stainless steel at cryogenic temperature[END_REF]. Depending on the value of the stacking fault energy (SFE), martensite can form directly or indirectly. For low SFE values (< 18 mJ/m 2 ), indirect transformation (γ → ε → α') occurs since formation of ε-martensite is easier in this case, while high SFE (> 18 mJ/m 2 ) causes direct transformation (γ → α') [START_REF] Allain | Correlations between the calculated stacking fault energy and the plasticity mechanisms in Fe-Mn-C alloys[END_REF][START_REF] Kaoumi | Deformation induced martensitic transformation in 304 austenitic stainless steel: In-situ vs. ex-situ transmission electron microscopy characterization[END_REF][START_REF] Talonen | Formation of shear bands and strain-induced martensite during plastic deformation of metastable austenitic stainless steels[END_REF]. The value of SFE depends on the chemical composition, elastic strain, temperature and magnetic contribution [START_REF] Talonen | Formation of shear bands and strain-induced martensite during plastic deformation of metastable austenitic stainless steels[END_REF], [START_REF] Wan | The influence of temperature on stacking fault energy in Fe-based alloys[END_REF]. α'martensite possesses a higher strength than ε-martensite [START_REF] Christ | Metastable Austenitic Stainless Steels and the Effect of Deformation-Induced Phase Transformation on the Fatigue Properties[END_REF] and its existence can improve the material properties such as yield stress and fatigue limit.

As martensitic transformation is one of the main parameters that can affect the fatigue behavior of austenitic stainless steel, its effect should be taken into account. Although, a considerable amount of research has been carried out on the fatigue life of this material during the last 25 years [START_REF] Colin | Fatigue Behavior of Stainless Steel 304L Including Strain Hardening, Prestraining, and Mean Stress Effects[END_REF][START_REF] Gupta | Prestraining Induced Enhancement in the Fatigue Limit Obtained by Load Increasing Thermal Method for Metastable Austenitic Stainless Steel[END_REF][START_REF] Kamaya | Mean stress effect on fatigue strength of stainless steel[END_REF][START_REF] Le Roux | Cyclic Deformation and Fatigue Behaviors of Stainless Steel 304L Including Mean Stress and Pre-Straining Effects[END_REF]Liu et al., 2018;Müller-Bollenhagen et al., 2010a;[START_REF] Nakajima | Coaxing Effect in Stainless Steels and High-Strength Steels[END_REF][START_REF] Paquet | Characterizing the effect of residual stresses on high cycle fatigue (HCF) with induction heating treated stainless steel specimens[END_REF][START_REF] Vincent | On the high cycle fatigue behavior of a type 304L stainless steel at room temperature[END_REF], the influence of phase transformation on high cycle fatigue behavior has been examined to a lesser extent [START_REF] Wu | Characterization of a Metastable Austenitic Stainless Steel with Severe Plastic Distortions[END_REF][START_REF] Zeng | Mechanical behavior and fatigue performance of austenitic stainless steel under consideration of martensitic phase transformation[END_REF].

Since, the traditional methods for fatigue characterization are extremely time consuming and costly, several alternative methods have been developed to allow a fast assessment of fatigue properties such as the ultrasonic fatigue test [START_REF] Bortoluci Ormastroni | LCF, HCF and VHCF life sensitivity to solution heat treatment of a third-generation Ni-based single crystal superalloy[END_REF][START_REF] Grigorescu | Cyclic deformation behavior of austenitic Cr-Ni-steels in the VHCF regime: Part I -Experimental study[END_REF][START_REF] Torabian | Correlation of the high and very high cycle fatigue response of ferrite based steels with strain rate-temperature conditions[END_REF] and other methods [START_REF] Charkaluk | Dissipative aspects in high cycle fatigue[END_REF][START_REF] Dengel | Estimation of the fatigue limit by progressively-increasing load tests[END_REF][START_REF] Doudard | A probabilistic two-scale model for highcycle fatigue life predictions[END_REF][START_REF] Meneghetti | A two-parameter, heat energy-based approach to analyse the mean stress influence on axial fatigue behaviour of plain steel specimens[END_REF][START_REF] Ricotta | Comparison of Experimental Thermal Methods for the Fatigue Limit Evaluation of a Stainless Steel[END_REF][START_REF] Risitano | Determining fatigue limits with thermal analysis of static traction tests[END_REF]. One of the most robust methods for fast evaluation of the fatigue properties of different materials is the self-heating (SH) test, which is based on the assessment of the material temperature variations that occur under cyclic loadings.

Since, cyclic loading is an energy-dissipating mechanism, it is accompanied by a rise in temperature in the material. The SH method is based on the measurement of the temperature elevation at the surface of the specimen as a result of the intrinsic dissipation due to the microplasticity phenomenon [START_REF] Munier | Identification of the micro-plasticity mechanisms at the origin of self-heating under cyclic loading with low stress amplitude[END_REF]. In this method, successive cyclic loading tests are performed with increasing stress amplitudes and the temperature evolution relevant to each stress amplitude is registered. Finally, the SH curve is obtained by plotting stabilized mean temperature (which is determined for each loading block) versus stress amplitude. This method allows the endurance limit of a material to be determined using only one sample and a couple of hours of testing, instead of weeks or even months of tests using a considerable amount of samples in order to complete an S-N fatigue curve. The SH method has proved to be an efficient, fast technique for determining the fatigue endurance limit of different alloys such as steels [START_REF] Krapez | Thermography detection of early thermal effects during fatigue tests of steel and aluminum samples[END_REF][START_REF] Krapez | Lock-in thermography and fatigue limit of metals[END_REF][START_REF] Louge | Apports des mesures d'auto-échauffement pour l'étude de la fatigue des aciers : effets d'histoire et cisaillement[END_REF][START_REF] Munier | Determination of high cycle fatigue properties of a wide range of steel sheet grades from self-heating measurements[END_REF][START_REF] Munier | Towards a faster determination of high cycle fatigue properties taking into account the influence of a plastic pre-strain from selfheating measurements[END_REF], titanium TA6V [START_REF] Roué | Rapid determination of the high cycle fatigue properties of high temperature aeronautical alloys by selfheating measurements[END_REF], chrome-cobalt [START_REF] Doudard | Influence of hardening type on self-heating of metallic materials under cyclic loadings at low amplitude[END_REF], aluminum 7010, 2024 [START_REF] Krapez | Thermography detection of early thermal effects during fatigue tests of steel and aluminum samples[END_REF] and A7N01 [START_REF] Zhang | Rapid determination of fatigue life based on temperature evolution[END_REF], copper-aluminum [START_REF] Ezanno | A new approach to characterizing and modeling the high cycle fatigue properties of cast materials based on self-heating measurements under cyclic loadings[END_REF], shape memory alloys (SMAs) [START_REF] Mostofizadeh | Fatigue analysis of shape memory alloys by self-heating method[END_REF], composites [START_REF] Abello | Fast Prediction of the Fatigue Behavior of Short Fiber Reinforced Thermoplastics from Heat Build-up Measurements[END_REF] and elastomers [START_REF] Masquelier | Determination of dissipated energy fields from temperature mappings on a rubber-like structural sample: Experiments and comparison to numerical simulations[END_REF]. However, it has not yet been applied to materials with irreversible phase transformation such as metastable austenitic stainless steels, which would experience a martensitic transformation under thermomechanical loadings.

In the case of austenitic stainless steel, phase transformation can influence fatigue behavior and the SH measurements can contribute to a better understanding of simultaneous microplasticity and martensitic transformation mechanisms during cyclic loading. For other materials that experience phase transformation such as SMAs, the predicted endurance limit using the self-heating method is in good agreement with the results obtained by classic fatigue tests [START_REF] Mostofizadeh | Fatigue analysis of shape memory alloys by self-heating method[END_REF]. This fact is encouraging considering the complexity of martensitic transformation. Nevertheless, unlike SMAs, martensitic transformation is irreversible in the context of metastable austenitic stainless steels. However, the capability of the SH method to predict the fatigue limit of austenitic stainless steel should be investigated as it is not in the scope of this paper.

This study focuses on the SH response of the austenitic stainless steel 304L and the effect of different parameters and initial states of the material on SH curves is investigated. As far as we are aware, there is no study in the literature about SH and high cycle fatigue behavior of this material at low temperatures, which reflects the importance of this study. This paper is subdivided into three main parts. Firstly, the mechanical behavior of the studied material at different temperatures ranging from -130°C to 100°C is determined. In the second part, the SH test procedure and underlying assumptions of the 0D approach details are fully explained. In addition, the effect of different parameters such as (i) the testing temperature, (ii) the pre-strain (PS) at room temperature (RT) and (iii) the initial volume fractions of martensite (VFM) are examined. This pre-existing martensite can affect the yield stress as well as the SH behavior of the material. It is worth noting that this is the first time that the effect of VFM on SH behavior is decoupled from its effect on yield stress. Finally, microstructural observations are performed using FERITSCOPE, scanning electron microscopy (SEM) and electron backscatter diffraction (EBSD) to determine the different initial states of the material as well as the microstructural evolutions after SH tests.

Material specifications

Studied material

The material examined in this study is 304L austenitic stainless steel. The chemical composition of this material is given in Table 1. Based on the chemical composition, there are multiple empirical formulas to estimate the austenite stability via specific parameters such as the martensite start temperature (MS) and the SFE. The values calculated for the MS and SFE using various equations from the literature [START_REF] Hahnenberger | Microstructural investigation of the fatigue behavior and phase transformation in metastable austenitic steels at ambient and lower temperatures[END_REF][START_REF] Schramm | Stacking fault energies of seven commercial austenitic stainless steels[END_REF][START_REF] Smaga | Investigation and modelling of the plasticity-induced martensite formation in metastable austenites[END_REF] are about -181°C and 26 mJ/m 2 , respectively.

To prepare the specimens, cylinders of 30 mm diameter were extracted from bulk material by water jet cutting. Before machining, in order to eliminate the internal stresses and the history effects due to the manufacturing process, these cylinders were annealed at T=1050°C for 10 minutes using argon gas and then, quenched in water. After this heat treatment, the material becomes pure austenite [START_REF] Christ | Metastable Austenitic Stainless Steels and the Effect of Deformation-Induced Phase Transformation on the Fatigue Properties[END_REF]. Figure 1 shows a homogeneous and purely austenitic microstructure. This microstructure consists of polygonal austenitic grains with some annealing twins. The average grain size of the heat-treated material is about 100-150 μm. The heat-treated cylinders were then machined to obtain the final shape of the specimens. This specimen shape was designed to allow the use of mechanical fixtures in the thermal chambers and to apply tensioncompression loadings. The specimen geometry is depicted in Figure 2.

Experimental setup

Uniaxial tensile and SH tests were carried out using a servo-hydraulic traction-torsion-compression (TTC) machine with a load capacity of ±100kN. The strain was measured by an Epsilon axial extensometer with a gauge length of 25 mm and a working temperature range of between -270°C and 100°C. Moreover, to measure the temperatures, three T-type thermocouples were taped onto the center of the sample and the lower and the upper jaws of the testing machine.

To conduct the tests at different temperatures using the thermal chambers, special jaws were designed enabling the application of tension-compression loading. An electrical thermal chamber was used to perform the tests at temperatures ranging from -50°C to 100°C and a cryogenic chamber fed by liquid nitrogen was employed for lower temperatures down to -130°C. This experimental setup is shown in Figure 3. performed on an AZTEC system provided by OXFORD Instruments. EBSD was carried out at two different magnifications of 150 × and 350 × and the step size chosen for each magnification was of 0.7 μm and 0.5 μm, respectively. In addition, the number of grains analyzed was about 80. Three different areas through the gauge length (one area in the middle and two others near the border of the gauge length) were scanned for each specimen to improve the statistical analysis. EBSD analysis was used to identify the phase fractions and their distribution on the one hand and to determine the crystallographic orientations and morphology on the other hand.

For EBSD analysis, samples need meticulous preparation. The samples were mechanically polished through different steps, finishing with an oxide polishing suspension (OP-S) up to 0.04 μm.

The ferrite content was measured using a FERITSCOPE FMP30, which is based on the magnetic induction method. By this method, paramagnetic austenite can be separated from ferromagnetic α'martensite. Since the FERITSCOPE was calibrated to measure the ferrite content, it was necessary to convert these magneto-inductive values to α'-martensite. A multiplication factor was identified in accordance with (Müller-Bollenhagen et al., 2010a;[START_REF] Talonen | Comparison of different methods for measuring strain induced α-martensite content in austenitic steels[END_REF]) by fitting the results obtained and the VFM determined by EBSD analysis. The value of the identified factor was 1.2 in this study.

Mechanical properties of the material

A uniaxial tensile test was performed at RT (~ 20°C) under a strain rate of 0.025% s -1 in accordance with DIN EN ISO 6892-1 until failure (Figure 4). The strain rate plays an important role in austenitic stainless steel since changes to the rate affect the mechanical behavior and microstructural evolution. Several researchers have examined the effect of this parameter and have shown that by increasing the strain rate, the yield stress increases, while the ultimate tensile stress and the VFM decrease [START_REF] Acharya | Effect of high strain rate deformation on the properties of SS304L and SS316LN alloys[END_REF][START_REF] Das | Morphologies and characteristics of deformation induced martensite during tensile deformation of 304 LN stainless steel[END_REF][START_REF] Haušild | Characterization of strain-induced martensitic transformation in a metastable austenitic stainless steel[END_REF][START_REF] Hedström | Load Partitioning and Strain-Induced Martensite Formation during Tensile Loading of a Metastable Austenitic Stainless Steel[END_REF][START_REF] Shen | Twinning and martensite in a 304 austenitic stainless steel[END_REF]. At high strain rate, the material cannot completely dissipate the heat induced by deformation, so there is enough heat to inhibit transformation. In addition, this heat reduces the nucleation sites and eventually the volume fraction of α'-martensite [START_REF] Hecker | Effects of Strain State and Strain Rate on Deformation-Induced Transformation in 304 Stainless Steel: Part I. Magnetic Measurements and Mechanical Behavior[END_REF][START_REF] Talonen | Effect of strain rate on the strain-induced γ → α′-martensite transformation and mechanical properties of austenitic stainless steels[END_REF]. In this study for quasi-static tests, the strain rate considered was low enough not to inhibit martensitic transformation.

The VFM was measured using the FERITSCOPE during the tensile test and as one can see in Figure 4, the amount of martensite formation monotonically increased with increasing strain. The VFM after failure of the specimen was about 0.9%. As high nickel content enhances austenite stability, the material studied, which contained 9.32% nickel underwent a limited amount of martensitic transformation at RT even at high deformation due to the stability of the austenite. Hence, the material studied was not metastable at RT [START_REF] Christ | Metastable Austenitic Stainless Steels and the Effect of Deformation-Induced Phase Transformation on the Fatigue Properties[END_REF]. The mechanical properties obtained from the 304L austenitic stainless steel are summarized in Table 2.

The yield strength is determined by an offset of 0.2%. A uniform elongation with final value of 78% and tensile strength of 617 MPa at RT are indicators of the high ductility of this material. In addition to strain rate, testing temperature can also significantly affect the mechanical properties and the martensitic transformation of the austenitic stainless steel. By decreasing the test temperature, the ultimate tensile strength, toughness and deformation-induced α'-martensite increase while elongation at fracture decreases [START_REF] De | Deformation-induced phase transformation and strain hardening in type 304 austenitic stainless steel[END_REF][START_REF] Hahnenberger | Influence of γ-α′-Phase Transformation in Metastable Austenitic Steels on the Mechanical Behavior During Tensile and Fatigue Loading at Ambient and Lower Temperatures[END_REF][START_REF] Liu | Use of in-situ TEM to characterize the deformation-induced martensitic transformation in 304 stainless steel at cryogenic temperature[END_REF]Müller-Bollenhagen et al., 2010b;[START_REF] Saint-Sulpice | Variation in electric resistivity in metastable alloys during thermomechanical loading: Effects of temperature, elasticity, plasticity and phase transformation[END_REF][START_REF] Zheng | Effect of low-temperature on mechanical behavior for an AISI 304 austenitic stainless steel[END_REF]. For more investigation, several uniaxial tensile tests until 30% strain were performed at different temperatures from -130°C up to 100°C. The effect of the testing temperature on the mechanical behavior of the material especially on the yield stress can be clearly seen in Figure 5 (a). This effect is amplified at temperatures of -90°C and -130°C, where a secondary hardening appears and the shape of the stress-strain curve changes to the sigmoidal form. As shown in Figure 5 (b), the yield stress at 0.2% decreased as the testing temperature increased, which is in good agreement with the findings of the literature [START_REF] Byun | Temperature dependence of strain hardening and plastic instability behaviors in austenitic stainless steels[END_REF][START_REF] Desu | Mechanical properties of Austenitic Stainless Steel 304L and 316L at elevated temperatures[END_REF][START_REF] Zheng | Effect of low-temperature on mechanical behavior for an AISI 304 austenitic stainless steel[END_REF]. Furthermore, after carrying out tensile tests at different temperatures, the volume fraction of α'-martensite was measured using the FERITSCOPE at seven different points through the gauge length for each specimen and an almost uniform distribution of α'-martensite was seen. These measurements will be discussed in detail in Section 4. Obviously, the volume fraction of α'-martensite increased with a decrease in the test temperature. This increase in α'-martensite was responsible for the hardening of the material [START_REF] Talonen | Comparison of different methods for measuring strain induced α-martensite content in austenitic steels[END_REF]. SH tests consist of a series of cyclic loading (or loading blocks) with increasing stress amplitude for the same specimen. At each stress amplitude, the cyclic loading is carried out with the same frequency and the number of cycles and the temperature elevation is recorded. There are two steps for each loading block; the first is the loading step (between time t0 and t1 in Figure 6) where the specimen is subjected to the specified number of cycles under sinusoidal load control condition. The second is a cooling step (between time t1 and t2), during which the cyclic loading is interrupted in order to cool the specimen down to the initial temperature (T0). This protocol is repeated for each loading block, and the temperature evolution relevant to each stress amplitude is recorded. When the temperature rise does not stabilize after achieving the desired number of cycles, the cyclic loading is stopped.

As a zero-dimensional (0D) approach was adopted (which will be detailed in the following), the mean value of the temperature field over the gauge length can be considered as the specimen temperature (Tspecimen). Since the temperature field is assumed to be homogeneous in this approach, the temperature of the specimen center is measured by the thermocouple. On the other hand, the temperature evolution in the jaws during cyclic loading may produce extra heating in the specimen. Therefore, to obtain the real temperature evolution of the specimen corresponding to the intrinsic thermal dissipation, the mean temperature of the jaws (1/2 × (Tupper jaw + Tlower jaw)) is subtracted from Tspecimen and the mean temperature change ( ), which is given by Equation ( 1), is registered during the test.

= - + 2 ⁄ (1)
The temperature rise reaches a stabilized value after a specific time (Figure 6). This stabilized mean steady state temperature ( ̅ ) is determined for each loading block and is plotted versus stress amplitude which is the so-called SH curve [START_REF] Doudard | A probabilistic two-scale model for highcycle fatigue life predictions[END_REF][START_REF] Munier | Determination of high cycle fatigue properties of a wide range of steel sheet grades from self-heating measurements[END_REF]. The temperature evolution during loading blocks with different stress amplitudes for the material studied is indicated in Figure 7; this SH test was performed at stress amplitudes of 50 up to 370 MPa (the stress amplitudes considered in this test are shown in Figure 8). All loading blocks were carried out with a loading ratio R= -1, a testing frequency (f) of 10 Hz and a number of cycles of 6000 per block. For the sake of clarity, only stress amplitudes between 140 and 370 MPa were plotted. This figure shows that the temperature increases rapidly at the beginning of the test (during the first 2000 cycles) and then it tends to reach a stationary value. This stabilization corresponds to a constant dissipated thermal source (i.e., a thermodynamic equilibrium between the heat loss with the surroundings and energy induced by mechanical loading). The higher stress amplitudes lead to the higher mean steady state temperature following the same trend until it reaches about 35°C for a stress amplitude of 350 MPa. At higher stress amplitudes, the temperature does not stabilize and it ramps up to 43°C after 6000 cycles. In contrast, for stress amplitudes between 50 MPa and 100 MPa, the evolution in temperature is negligible and for the values less than 140 MPa, it remains lower than 0.8°C. At the end of each loading step, the testing machine is stopped but temperature measurements continue for 400 seconds to record the cooling step (i.e., the temperature decrease in the specimen after having stopped the test). The SH curves on linear and logarithmic scale diagrams are shown in Figures 8a and8b, respectively. In these curves, the two last loading blocks (i.e. stress amplitudes of 360 MPa and 370 MPa), where the temperature evolution does not stabilize, are not considered.

From the logarithmic scale diagram, different SH regimes and their slopes can be identified. The number of regimes is different for various materials. For metals, generally two regimes exist [START_REF] Munier | Determination of high cycle fatigue properties of a wide range of steel sheet grades from self-heating measurements[END_REF], while for some composites e.g. short fiber reinforced thermoplastics, three regimes [START_REF] Abello | Fast Prediction of the Fatigue Behavior of Short Fiber Reinforced Thermoplastics from Heat Build-up Measurements[END_REF] and for austenitic steel of X4CrNiMoN 21-9-4, only one regime [START_REF] Puget | Influence du procédé sur la tenue à la fatigue des pièces forgées : application à une tige fémorale[END_REF] The energy dissipated from the material subjected to cyclic loadings generates a thermal field, the extent of which depends on different parameters such as the volume and the sample geometry, the material thermal properties, the thermal boundary conditions and the intensity of the thermal source due to the irreversible mechanisms. This generated heat leads to the material SH. In fact, the SH phenomenon is a representation of the energy dissipated in the material. The heat equation enables the relationship between the amount of dissipated energy and the corresponding SH magnitude to be established. The local form of the heat equation, which is derived from the principle of energy conservation, can be written as:

"# $ + %&'() *+ = ∆ + , + " -. / -0 - : 0$ + " -. / -2 3 - : 2 $ 3 = "#4 5 (2)
The left-hand side of Equation (2) defines the heat absorption ("# $ ) and the heat losses by conduction (%&'() *+). Where T, c, " and ) * are the temperature, the heat capacity, the density and the heat flux vector, respectively. The right-hand side of Equation ( 2) describes the local thermal source 4 5 , which consists of the intrinsic dissipated energy (∆= 6: 0$ -7 3 : 2 $ 3 ), the external heat supply (r) and the thermodynamic coupling source (" 8 9 : 8; < 8= : 0$ + " 8 9 : 8> ? 8=

: 2 $ 3 ). Where σ is the stress tensor, 0 is the elastic strain tensor, 0 is the plastic strain tensor, 7 3 denotes a set of thermodynamic forces associated to a set of the internal variables 2 3 and / is the Helmholtz free energy.

Since the temperature variations upon cyclic loadings can be considered to be small, one can assume that: c is independent of the temperature, the external heat supply is time-independent, the thermomechanical coupling source is negligible (i.e., " 8 9 : 8> ? 8=

: 2 $ 3 ~ 0) and the convective terms of the material time derivative are negligible (i.e., % %B ⁄ = --B ⁄ ). On the other hand, by supposing a homogenous temperature field throughout the volume of the specimen, the 0D approach can be considered (i.e. the thermal source is spatially homogeneous in the volume considered). By integrating Equation 2 over the volume and by considering the above-mentioned assumptions, one can obtain the following expression [START_REF] Doudard | Identification of heat source fields from infrared thermography: Determination of 'self-heating' in a dual-phase steel by using a dog bone sample[END_REF][START_REF] Doudard | A probabilistic two-scale model for highcycle fatigue life predictions[END_REF]: : 0$ ). By integrating the heat sources (4 5 ) over one cycle, the sum of thermoelastic coupling effects becomes null and the value of the average thermal source per cycle (4 ̅ 5 ) is given by:

$ (B+ + (B+ C D E = 4 5 (B+ (
$ F (B+ + F (B+ C D E = 4 ̅ 5 = G H 4 5 F %B = G "# ⁄ H ∆ F %B = G I "# ⁄ ( 4
)
where G is the loading frequency and F is the mean value of temperature evolution per cycle.

If the average value of heat source per cycle (4 ̅ 5 ) is constant, three different cases can be considered:

Case I. At the early beginning of each loading block (t = t0 = 0), the temperature evolution is negligible, i.e., F ~ 0 and based on Equation 4, $ F (B = t + = 4 ̅ 5 .

Case II. At the end of loading step of each loading block (where the temperature reaches a stabilized mean value, ̅ F ), the temperature rate is negligible, i.e., $ F ~ 0 and based on Equation 4,

̅ F = C D × 4 ̅ 5 .
Case III. At the beginning of the cooling step (where the loading is stopped in order to thoroughly cool down the specimen), the heat sources have vanished, i.e., 4 ̅ 5 = 0 and based on Equation 4, $ F (B =

B L + = -̅ F C D E .
It is expected that the SH curves obtained by these three methods lead to similar results. To investigate this claim, the SH curves of the previously mentioned test, are obtained by these three methods and the results are compared. In the first case, the SH curve can be extracted by fitting a line at t = t0 through the temperature-time curve for each loading block. The slope of the fitted line ( $ (t + obtained for the time range between 10 and 50 seconds in Figure 6) corresponds to the intrinsic dissipation. This temperature rate ( $ (t +) is determined for each loading block and it is plotted versus stress amplitude (green curve in Figure 10). This method has mostly been used for composite [START_REF] Abello | Fast Prediction of the Fatigue Behavior of Short Fiber Reinforced Thermoplastics from Heat Build-up Measurements[END_REF] and elastomer [START_REF] Masquelier | Determination of dissipated energy fields from temperature mappings on a rubber-like structural sample: Experiments and comparison to numerical simulations[END_REF] materials.

The stabilized average temperature rise, denoted by ̅ , is considered for plotting the SH curve in the second case. This ̅ is gained by averaging the temperature when it stabilizes (Figure 6). In this case, the intrinsic dissipation is calculated by dividing the stabilized mean temperature over the characteristic time. The characteristic time in the 0D approach depends on the dimensions of the specimen, the thermal conductivity of the material and the exchange coefficients between the jaws and the specimen and between the specimen and the environment. The least squares method is used to identify the characteristic time by fitting the experimental results on Equation 5 on the t1 to t2 part of the curve (Figure 6), where the temperature returns to its initial thermal state (T0). The characteristic time can be also obtained using the loading step (i.e., at the time between t0 and t1). In the loading step, the characteristic time depends on the loading frequency, hence, in this study, the second part (i.e., the cooling step) is used to obtain this characteristic time. Equation 5 is a solution of Equation 4, when levels (for the sake of clarity) in Figure 9. It would appear that the characteristic times obtained are constant. In the third case, the SH curve can be plotted by fitting a line at t = t1 through the temperature-time curve ( $ (t L + in Figure 6). This temperature rate ( $ (t L +) is determined for each loading block and is plotted versus the corresponding stress amplitude (pink curve in Figure 10). Since, the slope of the fitted line is negative in this case, its absolute value is considered in order to compare the results with those obtained in cases I and II.

Figure 10 indicates that the SH curves obtained by these three methods are in good agreement.

Consequently, in the rest of this study, the second method (the common one) will be used to plot the SH curves. After obtaining the SH curve, an empirical approach can be used to estimate the fatigue limit as shown in the literature [START_REF] Doudard | A probabilistic two-scale model for highcycle fatigue life predictions[END_REF][START_REF] Munier | Determination of high cycle fatigue properties of a wide range of steel sheet grades from self-heating measurements[END_REF]. In this method, the intersection of the asymptote at the two or three last points of the SH curve with the x-axis gives a good empirical estimation of the mean value of fatigue limit. The capability of this approach to predict the fatigue limit has been verified on a wide range of metals, by performing the classic fatigue tests, as mentioned in the introduction. In the case of austenitic stainless steel, this approach can be used as a fast and applicable method, but its results have yet to be verified. Confirming the fatigue limit obtained by this method with those gained using classic fatigue tests is out of the scope of this paper. In the following, this approach will be applied for a quantitative comparison of the fatigue limit values obtained under different conditions.

Influence of the loading frequency

As the loading frequency is an important parameter for the SH of the specimen, it is necessary to check its effect before studying the effect of other parameters. To this end, three different frequencies of 3 Hz, 10 Hz and 20 Hz are considered. The SH curves obtained on the linear and logarithmic scale diagrams are shown in Figures 11a and11b, respectively. Based on Equation 4, the loading frequency is a parameter that can modify the thermal source. Therefore, increasing the loading frequency amplifies the stabilized mean temperature of the material. Hence, in this section, the stabilized mean temperature is normalized by dividing the temperature rise over the loading frequency. It can be noted that the SH curves obtained for all frequencies are in good agreement. Thus, the evolution of stabilized mean temperature can be considered as a linear function of the frequency, similar to other metals [START_REF] Munier | Determination of high cycle fatigue properties of a wide range of steel sheet grades from self-heating measurements[END_REF]. It means that the intrinsic dissipation source of SH in the material studied is nearly constant. Since, the frequency does not have a notable effect on the SH results, in the following, the frequency of 10Hz and the number of cycles equal to 6000 are considered for each loading block. In addition, all tests were carried out under load control and R=-1.

Influence of the testing temperature

One of the important parameters for investigating the SH behavior of the austenitic stainless steel could be the temperature at which the tests have been performed. Figures 12a and12b show the results of SH tests at three different temperatures such as RT (~ 20°C), 0°C and -30°C on linear and logarithmic scale diagrams, respectively. The environment temperature was controlled by a thermal chamber during these tests and the temperature inside the chamber was kept constant. By decreasing the test temperature from RT to -30°C, the mechanical properties of the material seem to be improved as mentioned before. For instance, the yield stress of the material increased from 270 MPa to 357 MPa. Therefore, the specimen needs a higher stress amplitude value to achieve the same amount of intrinsic dissipation (e.g. for the stabilized mean temperature of 4.4°C (Figure 12a), the stress amplitudes of 185 MPa, 205 MPa and 220

MPa are required at testing temperatures of 20°C, 0°C and -30°C, respectively). Hence, the SH curves shifted to the right, which could mean that the fatigue limit of the material is improved by decreasing the testing temperature.

After the SH test, the VFM was measured using the FERITSCOPE and the maximum value of α'martensite for these tests was lower than 0.5%. Since, in the SH test procedure, the stress must stay lower than the yield strength, there was not enough mechanical driving force to start the martensitic transformation [START_REF] Krupp | Deformation-induced martensite formation during cyclic deformation of metastable austenitic steel: Influence of temperature and carbon content[END_REF][START_REF] Talonen | Effect of strain-induced α'-martensite transformation on mechanical properties of metastable austenitic stainless steels[END_REF]. In addition, the SFE of the material studied was higher than 18 mJ/m 2 and as previously mentioned, in this case, the direct transformation happened through strain-induced transformation and not stress-induced transformation [START_REF] Shen | Twinning and martensite in a 304 austenitic stainless steel[END_REF].

Therefore, this low amount of martensite was predictable. As a conclusion from the results obtained, one can say that the martensitic transformation does not have a notable influence on the SH results and the improvement of the fatigue limit could be due to the temperature effect on the mechanical properties of the material.

The results in Figure 12b demonstrate that there is only one SH regime with identified slopes of 7.7 °C/MPa, 6.9 °C/MPa and 8 °C/MPa for the test temperatures of 20°C, 0°C and -30°C, respectively.

The slope of each curve is shown using the same color as the corresponding curve.

Influence of pre-strain at room temperature

In this section, the effect of PS at RT is investigated through SH tests. In order to study this effect, three different states of the material namely without PS (0% PS), with 15% PS and 30% PS were selected. As clearly shown in Figure 13a, the increase in the PS values at RT result in a shift of the SH curves to the right. This could imply improvement in the fatigue life. These results are in accordance with those presented by [START_REF] Gupta | Prestraining Induced Enhancement in the Fatigue Limit Obtained by Load Increasing Thermal Method for Metastable Austenitic Stainless Steel[END_REF]. These authors stated that every 20% increment in pre-straining caused a 40 to 80 MPa enhancement in the fatigue life.

After these SH tests, the volume fractions of α'-martensite were measured using a FERITSCOPE and no quantifiable transformation was found even after performing an SH test on the 30% pre-strained specimen. These results are in line with the findings of [START_REF] De | Deformation-induced phase transformation and strain hardening in type 304 austenitic stainless steel[END_REF], stating that the deformation at RT does not initiate any measurable transformation up to 30% strain. Therefore, it should be noted that these curves show the influence of the plastic strain and not the effect of the martensitic transformation.

Figure 13b depicts the SH curves at three PS levels on the logarithmic scale. One SH regime with different slopes is illustrated for these three PS levels. The slope of the SH curve without PS is 7.7 °C/MPa, while for the pre-strained samples (i.e., 15% PS and 30% PS) it is 4 °C/MPa and 3.7 °C/MPa, respectively.

Influence of a complex thermomechanical history

As previously stated, no martensitic transformation occurred during the SH tests performed on the virgin specimens at different temperatures and on the pre-strained specimens at RT. Therefore, to study the effect of martensite fraction on the SH behavior, two different material initial states were considered:

One state along with martensitic transformation (case 1 in Figure 14 (a)) and another without martensitic transformation (case 2 in Figure 14 (a)). On the one hand, for temperatures higher than Ms (the martensite start temperature) with sufficient mechanical driving force that is supplied by applying stress or strain, martensitic transformation can occur [START_REF] Christ | Metastable Austenitic Stainless Steels and the Effect of Deformation-Induced Phase Transformation on the Fatigue Properties[END_REF][START_REF] Krupp | Deformation-induced martensite formation during cyclic deformation of metastable austenitic steel: Influence of temperature and carbon content[END_REF]. Therefore, several tensile tests up to 30% strain were performed at a wide range of temperatures between -130°C to RT (case 1 in Figure 14 (b)). Hence, there was a material state with the same inelastic strain but different VFM (due to different PS temperatures). Then, the SH tests at RT were conducted on these pre-strained specimens (case 1 in Figure 14 (c)). On the other hand, for temperatures higher than Md (i.e., the maximum temperature at which martensitic transformation can be induced by plastic deformation), there was no phase transformation due to high SFE and a low chemical driving force [START_REF] Hedström | Load Partitioning and Strain-Induced Martensite Formation during Tensile Loading of a Metastable Austenitic Stainless Steel[END_REF][START_REF] Olson | A mechanism for the strain-induced nucleation of martensitic transformations[END_REF][START_REF] Sugimoto | Fracture strength and toughness of ultra high strength TRIP aided steels[END_REF] and hardening was only due to plastic strain. Thus, after applying 30% PS at 100°C (case 2 in Figure 14 (b)) and subsequently performing an SH test at RT on this pre-strained specimen (case 2 in Figure 14 (c)), the VFM was almost zero. Therefore, by using this method and comparing the results obtained from these two cases, the effect of the martensite fraction can be studied on the SH curves. trend can be seen. Since, for the material with the same inelastic strain, lower temperatures lead to higher VFM and given that, the martensite phase has a higher strength than the austenite, a secondary hardening in tensile curves can appear, which is schematically shown in case 1 in Figure 14 (b). This secondary hardening causes an improvement in the mechanical properties and the fatigue limit of the material [START_REF] Gupta | Prestraining Induced Enhancement in the Fatigue Limit Obtained by Load Increasing Thermal Method for Metastable Austenitic Stainless Steel[END_REF]Müller-Bollenhagen et al., 2010a;[START_REF] Shen | Twinning and martensite in a 304 austenitic stainless steel[END_REF][START_REF] Talonen | Comparison of different methods for measuring strain induced α-martensite content in austenitic steels[END_REF]. Therefore, the secondary hardening relevant to pre-straining at temperatures of -90°C and -130°C (Figure 5(a)) can be a reason for the shift of the corresponding SH curves to the right. On the other hand, in these curves, the effect of plastic strain and martensite fraction simultaneously exists and it is complex to explain their effects separately. Consequently, microstructural observations and further investigations are required to justify the origin of this particular trend and will be presented in the following sections. It is worth noting Since, applying 30% PS at different temperatures leads to changes in the yield stress of the material at RT, to identify this yield stress evolution, one can apply additional 10% PS at RT to the pre-hardened specimens up to 30% at different temperatures. In Figure 16 (a), the stress-strain curves obtained during 30% PS at different temperatures together with the stress-strain curves obtained by subsequently performing 10% PS at RT are shown. In this figure, the yield stress at RT after cold pre-straining is lower than that at low temperatures. For instance, the RT yield stress for the specimen pre-strained at -130°C is 906 MPa, which is lower than the corresponding stress value at -130°C (1111 MPa at the end of loading step). These evolutions could be due to the effect of temperature on the yield stress. In contrast, the yield stress at RT after hot pre-straining is higher than that at high temperature (i.e., 100°C). The evolution of the yield stress at RT after pre-straining at different temperatures is depicted in Figure 16 (b). As one can see in this figure, the yield stress at RT decreases by increasing the pre-straining temperature.

Moreover, the slopes of stress-strain curves during the 10% PS at RT (shown in Figure 16 (a)) are approximately constant, while the corresponding slopes during 30% pre-straining at lower temperatures progressively increase, especially at higher strain values (i.e., strain values between 20% and 30%). This increase in the slope of the stress-strain curves at lower temperatures is due to martensitic transformation, which caused secondary hardening (e.g., at temperatures of -90°C and -130°C). Thus, one can state that the constant slope of stress-strain curves at RT is more due to plasticity. Hence, by eliminating the evolution of the yield stress, one can investigate the effect of the martensite fraction on the SH curves.

Microstructure evolution analysis

The VFM after applying PS at different temperatures was measured using a FERITSCOPE at seven different points with a distance of 5mm from each other through the gauge length (which is shown schematically in Figure 18) and an almost uniform distribution of martensite is seen. In Figure 18, dash lines demonstrate the VFM measured after 30% PS at different temperatures. In addition, after each SH test at RT, the VFM was measured once again and no significant change was seen (solid lines in Figure 18). One can note that the VFM increases by decreasing the test temperature. shear bands appear in a few austenitic grains. These initial shear bands are parallel to each other and nucleate more at grain boundaries. By decreasing the temperature, they grow more into the austenite grain. At temperatures less than -30°C, the nucleated shear bands intersect each other, which is due to the activation of the secondary slip systems [START_REF] Hedström | Load Partitioning and Strain-Induced Martensite Formation during Tensile Loading of a Metastable Austenitic Stainless Steel[END_REF] and some dark areas arise, which can be considered as martensite. These dark areas are more visible in the junction of shear bands with grain boundaries or twins at temperatures of -30°C and -50°C, while at lower temperatures, they cover most of the austenite grains. represented by red, yellow and blue colors, respectively. To obtain the actual value of the volume fraction of phases, the selected area was sufficiently large. Mean Angular Deviation (MAD) was less than 1°, which shows a good match between the Kikuchi bands detected and the simulation. The "zero solutions" points that originate from non-indexing pixels were lower than 3%. As one can see in these figures, at temperatures of RT and 0°C, there is no significant amount of α'-martensite, while at temperatures of -30°C and -50°C, the amount of α'-martensite increases, as observed in some grains. By decreasing the temperature to -90°C and -130°C, α'-martensite increasingly covers the grains as previously observed by [START_REF] Hedström | Load Partitioning and Strain-Induced Martensite Formation during Tensile Loading of a Metastable Austenitic Stainless Steel[END_REF] who stated that for VFM higher than 25%, a continuous network of martensite is created. It can be observed that α'-martensite forms at the inner of twins and close to the grain boundaries and the martensite which forms is in the shape of needles. The measured volume fraction of α'-martensite was 0.06%, 0.15%, 11.36%, 14.12%, 40.16% and 46.01% at temperatures of RT, 0°C, -30°C, -50°C, -90°C and -130°C, respectively. One can state that for the same level of inelastic strain, the strain-induced martensite formation increases by decreasing the test temperature. It means that the amount of α'-martensite is a function of temperature and PS. The VFM at a temperature of 100°C, which is quantified by EBSD and FERITSCOPE, is around 0%. Therefore, the Md temperature of the material studied is between RT and 100°C.

The amount of ε-martensite determined for all the cases is less than 0.6%. As previously mentioned, for SFE higher than 18 mJ/m 2 , direct transformation occurs; since the SFE of the material studied is about 26 mJ/m 2 , therefore, direct transformation is expected and in this case there is no intermediate phase (i.e., εmartensite). That is the reason for the low values of ε-martensite that were observed in this study. The VFM measured by the FERITSCOPE shows good agreement with those obtained by EBSD (Figure 21). Based on the VFM measured in this section, one can state that for the amount of α'-martensite between 0.09% and 15%, the behavior of the material in terms of SH response is similar (Figure 15) and represent a decrease in the fatigue life. On the contrary, for α'-martensite values higher than 15% (i.e., 40% and 45%), an inverse behavior can be seen that could demonstrate an increase in the fatigue life. This increase in the fatigue limit may be due to the TRIP effect, which can strengthen the material and cause the appearance of a secondary hardening. Therefore, the optimal value of VFM for the material studied is higher than 15%. Classic fatigue tests with varying values of VFM will be performed to verify the determined optimal value of VFM in the continuation of the present work. (b) Supposing a constant thermal source during cyclic loading, three methods can be considered to assess the SH response of the material. The results obtained from these three methods were almost in good agreement, which proved that the initial assumption was correct. Moreover, the procedure to obtain the characteristic time, which represents heat loss to the surroundings, was fully described.

(c) Investigating the effect of the test temperature indicated that the SH curves shifted to the right with a decrease in the testing temperature. This could mean that the fatigue properties were improved by decreasing the testing temperature. (e) Decreasing the temperature to within a band of 100°C to -50°C moved the SH curves to the left, whilst decreasing the temperature to within a band of -90°C to -130°C moved the curves to the right.

Consequently, one can say that the optimum values (in respect of fatigue life improvement) of VFM for the material studied were higher than 15%. By normalizing the stress amplitude over the RT yield stress, the effect of the initial VFM on the SH behavior was decoupled from its effect on the yield stress. The results have led us to conclude that for PS temperatures lower than -50°C, the effect of martensitic transformation on the SH curves was identical. In other words, for VFM between about 15% and 45%, the SH behavior of material was the same.

(f) The VFM measured after all the SH tests showed that there is no phase transformation due to cyclic loading below the macroscopic yield stress.

This study represents a crucial first step toward the fatigue study of stainless steel materials using the SH method. Future work will concentrate on performing classic fatigue tests to confirm the conclusions made by conducting the SH tests.

Fig. 1 .

 1 Fig. 1. Microstructure of heat-treated material

Fig. 2 .

 2 Fig. 2. Specimen geometry (dimensions in mm)

Fig. 3 .

 3 Fig. 3. Experimental setup for the controlled environment temperature tests For microstructural observations, a JEOL JSM-IT300LV Scanning Electron Microscope (SEM) equipped

Fig. 4 .

 4 Fig. 4. Engineering stress-strain curve and VFM versus strain

  (a) Uniaxial tensile tests at different temperatures until 30% strain (b) evolution of yield stress versus temperature

Fig. 6 .

 6 Fig. 6. Temperature and stress evolution versus time during one loading block

Fig. 7 .

 7 Fig. 7. Mean temperature evolution during different cyclic loading blocks

  are observed. For the material studied at room temperature (on the specimen with or without PS) and at low temperatures, one SH regime is always observed. The SH curve on the logarithmic scale plus or minus the precision error ( ± ∆ ) of the thermal measurements with the thermocouple (∆ = 0.1 °C) is plotted in Figure 8b (i.e., green curves). Since the slopes of the regimes are an indicator for the SH phenomenon (Munier et al., 2014), their calculation is important. As it is clear in this figure, there is only one SH regime with a slope value of 3.6 °C/MPa. (a) (b) Fig. 8. SH curve on (a) linear (b) logarithmic scale diagrams After describing the testing process, in the following, more details about the 0D approach and different post-processing methods of the SH tests are discussed.

  3) where is the elevation of the mean temperature in the volume, C D is a characteristic time representing heat losses with the surroundings and 4 5 is the mean value of the thermal source throughout the material volume, which can be broken down into an intrinsic dissipation and a thermoelastic coupling term (i.e., "

F

  Fig. 9. (a) Identification of characteristic time (C D ) using the cooling part of the temperature-time curves (b)table of the values obtained from curve fitting

  Comparison of SH curves obtained from three different methods on (a) linear (b) logarithmic scale diagrams

  . SH curves obtained with different loading frequencies on (a) linear (b) logarithmic scale diagrams

  . SH curves at different temperatures on (a) linear (b) logarithmic scale diagrams

  . SH curves after different PS levels on (a) linear (b) logarithmic scale diagrams

  . Schematic illustration of (a) pseudo-diagram of metastable materials with the loading paths considered (b) conducting PS at different temperatures (c) performing the SH tests at RT on the pre-strained specimens The SH curves at RT obtained on pre-strained specimens are demonstrated in Figure 15(a). As one can see in this Figure, by decreasing the test temperature, there are two different trends. From 100°C up to -50°C, the SH curves shifted to the left, and with a further decrease from -90°C to -130°C, an inverse

  that only one SH regime with a slope of about 3 °C/MPa is observed for these pre-strained specimens on a logarithmic scale (Figure15(b)).(a) (b) Fig. 15. SH curves with different volume fractions of martensite on (a) linear (b) logarithmic scale diagrams

  Fig. 17. SH curves after normalization of stress amplitude on (a) linear (b) logarithmic scale diagrams

Fig. 18 .

 18 Fig. 18. Volume fraction of α'-martensite measured using FERITSCOPE after 30%PS at different temperatures and after SH tests at RT on pre-strained specimensTo confirm the volume fraction of α'-martensite obtained using the FERITSCOPE, EBSD analysis was

  Fig. 19. Band contrast maps after SH tests at RT on the pre-strained specimens at temperatures of (a) RT (b) 0°C (c) -30°C (d) -50°C (e) -90°C (f) -130°C To prove our supposition that the dark areas are a martensite, phase maps are used. These maps display the distribution of the different phases in the microstructure. Figures 20(a) to (f) show the phase maps of pre-strained specimens after SH tests at RT. α'-martensite, ε-martensite and austenite phases are

  . Volume fraction of phases after SH tests at RT on the pre-strained specimens at temperatures of (a) RT (b) 0°C (c) -30°C (d) -50°C (e) -90°C (f) -130°C

Fig. 21 .

 21 Fig. 21. Comparison of the VFM measured by FERITSCOPE and EBSD after SH tests at RT on the pre-strained specimens5. Conclusion

  (d) Increasing the PS values at RT resulted in the SH curves shifting to the right. This could imply an improvement in the fatigue properties.

Table 1 .

 1 Chemical composition of stainless steel 304L (wt. %)

	C	Mn	P	S	Si	Cr	Ni	N	Mo	Cu	Iron
	0.029	1.89	0.028 0.001	0.33	18.20	9.32	0.08	0.26	0.28 Balance

Table 2 .

 2 Mechanical properties of 304L austenitic stainless steel

	Material	Young's modulus (GPa)	R 0.2% (MPa)	Tensile strength (MPa)	Elongation after fracture (%)
	Stainless steel 304L	201	271	617	78

= 0 (i.e., during the cooling step). The results of this identification are presented for six loading

Acknowledgments

We kindly acknowledge the Region Bretagne, France, for partly financing the PhD scholarship of Behnaz Amini.


Guillaume Labbé

Carole Egron

André Labbé
email: labbe.andre@wanadoo.fr

Le tabagisme passif chez l'enfant et les risques allergiques

Keywords: tabac, grossesse, inhalation passive, asthme, allergie

Le tabagisme passif chez l'enfant et les risques allergiques. Passive smoking in children and allergic risk RESUME Le tabagisme pré et post natal a des conséquences sur le développement pulmonaire, modifie la réponse immunitaire et augmente la prévalence des bronchites sifflantes durant l'enfance. Les nouveau-nés exposés ont un risque d'altération de leur fonction respiratoire et d'augmentation des symptômes d'asthme. Récemment les progrès de la génomique et de l'épigénétique ont mis en évidence des altérations de la méthylation de l'ADN pouvant expliquer des conséquences à long terme. Cette revue analyse l'influence du tabagisme passif sur l'augmentation des risques infectieux, la déviation de la réponse immunitaire vers un profil lymphocytaire de type TH2 et l'évolution vers un phénotype allergique des manifestations asthmatiques. Le tabagisme passif peut également contribuer au développement d'allergie alimentaire via la progression de la marche atopique, l'IPFT étant un risque avéré d'eczéma et d'asthme. Fumer pendant la grossesse est la cause la plus commune de morbidité et mortalité infantile que l'on peut prévenir. Il existe un faisceau d'argument qui montre que l'enfant peut aussi bénéficier pour sa santé de l'implantation d'une législation restreignant le tabagisme dans les lieux publics.

progression of the atopic march since SHS is a known risk factor for asthma and eczema. Smoking during pregnancy is the most common preventable cause of infant morbidity and mortality. There is an increasing body of evidence showing that children also reap health benefits following the introduction of legislation to restrict smoking in public places. Key words: tobacco, pregnancy, passive smoking, asthma, allergy Le tabagisme passif, surtout chez l'enfant, demeure un problème majeur de santé publique. Malgré les preuves accablantes de la nocivité de l'inhalation passive de fumée de tabac (IPFT) en pédiatrie, la réduction de l'exposition, à l'exception des lieux publics, demeure anecdotique, que ce soit durant la grossesse et après. Une analyse rétrospective (1) effectuée dans 192 pays en 2002 révèle que 40 % des enfants dans le monde sont exposés à la fumée d'une cigarette. 603.000 décès seraient attribuables au tabagisme passif, dont 28 % chez les moins de 16 ans [START_REF] Rojas-Rueda | Environmental Burden of Childhood Disease in Europe[END_REF]. Les études épidémiologiques récentes concernant l'environnement place le tabagisme passif comme facteur de risque de maladie chez l'enfant [START_REF] Peden | The "envirome" and what the practitioner needs to know about it[END_REF]. Il est encore inconcevable de constater qu'un pourcentage très important d'enfant de 7% en Finlande jusqu'à 34% en Italie est soumis à un tabagisme passif durant leur transport dans la voiture de leurs parents [START_REF] Mlinarić | Exposure to car smoking among youth in seven cities across the European Union[END_REF]. Cette gravité particulière de l'IPFT serait liée aux possibilités moindres de détoxification et à la quantité plus importante d'air respiré [START_REF] Cheraghi | Environmental tobacco smoke (ETS) and respiratory health in children[END_REF], notamment chez le petit enfant (0,53 m 3 /kg vs 0,2 m 3 /kg chez l'adulte). Les toxiques, par la possibilité d'interagir sur des niveaux de transcription des gènes, en particulier le tabac, sont capables de modifier la programmation de développement, notamment celui du poumon.

Samoliński et coll [START_REF] Samoliński | Council of the European Union conclusions on chronic respiratory diseases in children[END_REF], dans un éditorial de la Communauté Européenne pointent le tabagisme passif comme le facteur de risque principal des maladies respiratoires chroniques de l'enfant.

Cette revue se concentre sur les effets de l'IPFT sur la sphère respiratoire de l'enfant et l'impact qu'elle peut avoir sur la survenue de maladies allergiques, les conséquences allant bien au delà de ces deux systèmes (fig 1)

Toxicité de la fumée de tabac

En dehors de la nicotine, plus de 4 000 contaminants toxiques ont été individualisés dans la fumée de tabac. La combustion de la cigarette provoque la formation de très nombreux composés : goudron, gaz toxiques, métaux lourds, et beaucoup de substances irritantes. L'acroléine en fait partie [START_REF] Moretto | Acrolein effects in pulmonary cells: relevance to chronic obstructive pulmonary disease[END_REF]. Utilisée comme gaz de combat pendant la première guerre mondiale, cet aldéhyde alpha bêta insaturé est un irritant respiratoire abondant dans la fumée de tabac. Les concentrations peuvent varier de 0,006 à 0,120 PPM en atmosphère confinée. Parmi les effets indésirables de cette molécule, citons : le stress oxydatif, l'altération de gène de transcription, la production de médiateurs pro-inflammatoires, les modifications de la réponse immunitaire innée, l'altération de l'épithélium des voies aériennes et l'hyperproduction de mucus. On isole également dans l'air des maisons d'enfants exposés au tabac des métabolites de carcinogène pulmonaire, comme le 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanol [START_REF] Thomas | Metabolites of a tobacco-specific lung carcinogen in children exposed to secondhand or thirdhand tobacco smoke in their homes[END_REF]. Il est retrouvé dans les urines de 90 % des enfants soumis à l'inhalation passive de fumée de tabac.

Bio-marqueurs du tabagisme passif

L'appréciation objective du tabagisme passif n'est pas simple. A ce jour on ne dispose pas d'examen rapide (à la consultation par exemple) permettant d'apprécier quantitativement l'importance de cette inhalation, à l'exception des analyseurs de CO2 pour les parents. On en est réduit à se fier à l'interrogatoire des familles qui minimisent souvent cette pratique par crainte de remontrances ou de jugement négatif du corps médical. Le choix du site de prélèvement n'est pas anodin. Kalkbrenner AE et coll [START_REF] Kalkbrenner | Determinants of serum cotinine and hair cotinine as biomarkers of childhood secondhand smoke exposure[END_REF] rappellent que le dosage de cotinine (principal métabolite de la nicotine) est très influencé par le contexte racial. Florescu A et al [START_REF] Florescu | Reference values for hair cotinine as a biomarker of active and passive smoking in women of reproductive age, pregnant women, children, and neonates: systematic review and meta-analysis[END_REF] ont publié des valeurs de cotinine moyennes dans les cheveux en fonction du statut de fumeur (actif ou passif), et en fonction de l'âge (Tableau I).

Ils estiment qu'une valeur supérieure à 0,2 ng/mg, signe une exposition indiscutable. Il est clair qu'il existe une différence d'appréciation importante entre les dires des mamans et la réalité. C'est ce qu'ont prouvé Spanier AJ et al [START_REF] Spanier | Comparison of biomarkers and parent report of Tobacco exposure to predict wheeze[END_REF] qui ont suivi jusqu'à 2 ans une cohorte de 398 enfants pris en charge au deuxième trimestre de la grossesse. Sur les 367 examinés régulièrement avec des dosages de cotinine, 26 % étaient soumis au tabagisme passif d'après les parents, alors que 61 % étaient dépistés par des dosages sériques… On retrouve ces mêmes discordances quand on effectue des dosages sur le sang du cordon [START_REF] Puig | Assessment of prenatal exposure to tobacco smoke by cotinine in cord blood for the evaluation of smoking control policies in Spain[END_REF]. D'autres bio-marqueurs peuvent être utilisés pour analyser les conséquences sur l'appareil respiratoire (13). A ce titre, le dosage de la protéine de Clara (CC16) semble digne d'intérêt. Cette petite molécule, présente dans l'épithélium des voies aériennes distales (bronches et bronchioles), serait un bon reflet de l'intégralité épithéliale. Sa concentration augmente en cas d'agression, qu'elle soit d'origine toxique ou virale. St-Hélène G et coll [START_REF] St Helen | Utility of urinary Clara cell protein (CC16) to demonstrate increased lung epithelial permeability in nonsmokers exposed to outdoor secondhand smoke[END_REF] ont montré une augmentation significative des taux de CC16 après exposition au tabac dans des lieux publiques chez les femmes. Rabinovitch N et al [START_REF] Rabinovitch | Urinary leukotriene E4 identify children with Tobacco exposure at risk for asthma exacerbation[END_REF][START_REF] Rabinovitch | The response of children with asthma to ambient particulate is modified by tobacco smoke exposure[END_REF] ont pu également établir une corrélation entre les taux de leucotriènes urinaires E4, le risque d'exacerbation de l'asthme dans un groupe d'enfants asthmatiques traités par corticostéroïdes et soumis à un tabagisme passif. Cobanoglu M et al [START_REF] Cobanoglu | Is calprotectin a marker of tobacco smoke related inflammation?: a pilot study in children[END_REF] ont dosé la calprotectine (protéine appartenant à la famille des protéines 100ß impliquée dans les défenses de l'hôte) dans le sérum de 51 enfants non exposés comparés à 46 soumis au tabagisme passif. Les taux de calprotectine sont significativement plus élevés dans le groupe IPFT, traduisant l'inflammation liée à cette pollution domestique. L'utilisation de ces biomarqueurs pour essayer de diminuer le tabagisme passif est à l'étude notamment en utilisant ceux réputés carcinogènes comme le NNAL (4-[methylnitrosamino]-1-[3-pyridyl]-1-butanol) [START_REF] Thomas | Promoting smoke-free homes through biomarker feedback documenting child exposure to tobacco toxins : protocol for a randomized clinical trial[END_REF].

Tabac et grossesse

Dans une revue générale sur le tabagisme durant la grossesse, Abbot LC et al [START_REF] Abbott | Smoking during pregnancy: lessons learned from epidemiological studies and experimental studies using animal models[END_REF] décrivent les effets répertoriés : petit poids de naissance, augmentation des morts subites inexpliquées, troubles cognitifs, déficit de l'attention, augmentation de l'addiction. Léonardi-Bee J et al [START_REF] Leonardi-Bee | Secondhand smoke and adverse fetal outcomes in non smoking pregnant women: a meta-analysis[END_REF], dans une méta-analyse centrée sur les effets périnataux, montrent qu'il existe une augmentation des malformations congénitales dans 13 % des cas. La dérégulation de l'expression de gènes induite par l'exposition prénatale à la fumée de tabac (21,[START_REF] Gibbs | Impact of tobacco smoke and nicotine exposure on lung development[END_REF], bien décrite par Votava H et al [START_REF] Votavova | Deregulation of gene expression induced by environmental tobacco smoke exposure in pregnancy[END_REF][START_REF] Votavova | Transcriptome alterations in maternal and fetal cells induced by tobacco smoke[END_REF], explique probablement le caractère multifocal de l'agression. A l'appui d'un prélèvement sérique Ceci pourrait expliquer les effets à long terme, en particulier sur l'augmentation de la prédisposition à l'asthme. Il existe bien d'autres effets du tabagisme durant la grossesse (restriction pondérale, risque d'autisme et de dépendance…) qui ne sont pas abordé dans cette revue centrée sur l'appareil respiratoire. Rappelons que c'est bien la nicotine qui est responsable des effets sur le développement pulmonaire et qu'il est donc illusoire de proposer la e-cigarette durant la grossesse dans l'espoir de minimiser ses effets secondaires [START_REF] Mcevoy | Pulmonary effects of maternal smoking on the fetus and child: effects on lung development, respiratory morbidities, and life longlLung health[END_REF]. Les relations étroites entre la fréquence de la toux, les symptômes bronchiques ou l'asthme ont été clairement rapportées selon le degré d'exposition à la fumée de cigarette, qu'il s'agisse de jeunes enfants [START_REF] Burke | Prenatal and passive smoke exposure and incidence of asthma and wheeze : systematic review and meta-analysis[END_REF][START_REF] Duijts | Fetal exposure to maternal and paternal smoking and the risks of wheezing in preschool children :the generation R study[END_REF] ou d'adolescents [START_REF] Hedman | Both environmental tobacco smoke and personnal smoking is related to asthma and wheeze in teenagers[END_REF]. Elles sont mise en évidence quel que soit le pays concerné USA [START_REF] Hawkins | Increased tobacco exposure in older children and its effect on asthma and ear infections[END_REF] ou Japon [START_REF] Tanaka | Association between prenatal and postnatal tobacco smoke exposure and allergies in young children[END_REF] avec une exposition qui semble augmenter avec l'âge. Le tabagisme maternel a certainement un poids plus important que le tabagisme parental ou paternel. Cette prépondérance est précisée par l'étude de Duijts L et al [START_REF] Duijts | Fetal exposure to maternal and paternal smoking and the risks of wheezing in preschool children :the generation R study[END_REF] qui ont comparé le risque de sifflement de l'enfant d'âge scolaire en fonction du tabagisme maternel et paternel pendant la vie foetale. 4 574 enfants ont participé à ce suivi et ont été examinés à 1 an et 4 ans. C'est essentiellement le tabagisme continu maternel qui est associé aux risques de récurrence de sifflement avant 4 ans, sans que l'on puisse démontrer d'impact du tabagisme paternel sur ce paramètre. Que l'exposition soit pré ou postnatale, elle augmente de façon nette l'incidence de l'asthme chez l'enfant, surtout chez le nourrisson. Burke H et al [START_REF] Burke | Prenatal and passive smoke exposure and incidence of asthma and wheeze : systematic review and meta-analysis[END_REF] ont répertorié 79 études prospectives analysant les rapports entre tabagisme passif et l'incidence de l'asthme. Le risque de sifflement est augmenté de 30 à 80 % et celui de l'asthme de 21 à 85 %, avec une augmentation moyenne de l'incidence de 20 %. Chez les enfants asthmatiques, le risque d'exacerbation de leur maladie est largement influencé par IPFT. C'est ce que prouve le suivi prospectif sur 5 ans de 49 enfants d'âge scolaire sous corticostéroïdes [START_REF] Rabinovitch | Urinary leukotriene E4 identify children with Tobacco exposure at risk for asthma exacerbation[END_REF]. 45 % des enfants soumis à l'IPFT ont présenté une exacerbation, alors que seulement 12 % dans le groupe sans tabac en ont fait une. Dans cette même étude les auteurs ont montré que le taux de leucotriènes urinaires pourrait être un indicateur prédictif du risque d'aggravation (taux significatif plus élevé en cas de rechute), ce qui expliquerait les effets bénéfiques des antileucotriènes chez les enfants de parents fumeurs. Un élément important à considérer dans le suivi objectif des asthmatiques fumeurs passifs concerne le taux de NO exhalé. Le tabagisme passif diminue artificiellement les concentrations de NO expiré, si bien que l'on doit en tenir compte pour l'analyse de ce bio-marqueur [START_REF] De La | Relationship between exhaled nitric oxide and exposure to low-level environmental tobacco smoke in children with asthma on inhaled corticosteroids[END_REF][START_REF] Bobrowska-Korzeniowska | The effect of passive smoking on exhaled nitric oxide in asthmatic children M[END_REF]. Il faut également prendre en compte du tabagisme passif pour la réponse aux corticostéroïdes. Cohen RT et al [START_REF] Cohen | In utero smoke exposure and impaired response to inhaled corticosteroids in children with asthma[END_REF] ont bien montré une diminution nette de la réponse aux corticostéroïdes chez les enfants de 5 à 12 ans en analysant de façon répétée la réactivité à la métacholine. Les enfants exposés à la fumée de tabac ont une diminution de 26 % de la diminution de l'hyperactivité bronchique avec le temps, comparée à ceux qui ne sont pas exposés. Ceci pourrait expliquer, entre autre, le passage plus fréquent des enfants asthmatiques soumis au tabagisme passif aux services d'urgence. Ainsi pour 14 paramètres étudiés susceptibles d'expliquer une augmentation du risque de passage en unité de soins intensifs, van den Bosch GE et al [START_REF] Van Den Bosch | Risk factors for pediatric intensive care admission in children with acute asthma[END_REF], dans une analyse multivariée, en retiennent 4, dont le tabagisme passif ou actif avec l'allergie, les antécédents atopiques et les mauvaises conditions sanitaires à domicile. Comhair et al [START_REF] Comhair | Detrimental effects of environmental tobacco smoke in relation to asthma severity[END_REF] font le même constat.

Asthme et tabagisme passif

Maladies allergiques et tabac

Il est probable que le développement de maladies allergiques est facilité par le tabagisme [START_REF] Strzelak | Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases:A Mechanistic Review[END_REF]. [START_REF] Singh | Prenatal secondhand cigarette smoke promotes Th2 polarization and impairs goblet cell différentiation and airway mucuc formation[END_REF]. Cet effet est également retrouvé chez l'homme, avec une augmentation de l'expression des cytokines pro-inflammatoires IL-6, IL-8, TNF alpha [START_REF] Strzelak | Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases:A Mechanistic Review[END_REF]. Vardavas CI et al [START_REF] Vardavas | Passive smoking alters circulating naïve/memory lymphocyte T-cell subpopulations in children[END_REF] ont bien montré chez 68 adolescents non-fumeurs une réponse immunologique liée au tabagisme passif avec une augmentation des pourcentages de lymphocytes T naïfs et une diminution des pourcentages des lymphocytes T mémoire et des lymphocytes T killer. Les études récentes confirment cette augmentation du risque allergique en cas de tabagisme passif même si le risque relatif est faible [START_REF] Saulyte | Active or Passive Exposure to Tobacco Smoking and Allergic Rhinitis, Allergic Dermatitis, and Food Allergy in Adults and Children: A Systematic Review and Meta-Analysis[END_REF].

Si la fréquence des rhinites, de l'asthme ou de l'eczéma fait consensus, une publication originale met en évidence un risque accru d'allergie alimentaire à l'adolescence [START_REF] Feldman | Early-life secondhand smoke exposure and food hypersensitivity through adolescence[END_REF].L'équipe du centre de recherches médicales de Stockholm a suivi 3 764 enfants entre 1994 et 1996, jusqu'à l'âge de 16 ans.

Les familles étaient contactées à l'âge de 1, 2, 4, 8, 12 et 16 ans afin de savoir s'il existait des signes d'allergie alimentaire. A 4, 8 et 16 ans des tests de provocation à divers allergènes alimentaires étaient réalisés. Les enfants dont les parents fumaient depuis que l'enfant avait 2 mois étaient plus susceptibles de développer des signes d'allergie alimentaire, notamment à l'oeuf et à l'arachide.

Une prévention est-elle possible ?

Devant ce fléau que constitue l'inhalation passive de fumée de tabac chez l'enfant, il est important d'essayer de proposer de stratégies minimisant l'impact sur sa santé [START_REF] Rosen | Parental smoking cessation to protect Young children : a systematic review and meta-analysis[END_REF][START_REF] Hwang | Environmental tobacco smoke and children's health[END_REF][START_REF] Ortega | the BIBE study group. Passive smoking in babies: The BIBE study (Brief Intervention in babies. Effectiveness)[END_REF][START_REF] Kanoh | Longitudinal study of parental smoking habits and development of asthma in early childhood[END_REF][START_REF] Jung | Association between parental smoking behavior and children's respiratory morbidity: 5-year study in an urban city of South Korea[END_REF][START_REF] Treyster | Second hand smoke exposure in children: environmental factors, physiological effects, and interventions within pediatrics[END_REF][START_REF] Maas | Prevention of asthma in genetically susceptible children: a multifaceted intervention trial focussed on feasibility in general practice[END_REF] [START_REF] Bogdanovica | What factors influence smoking prevalence and smoke free policy enactment across the European Union Member States[END_REF][START_REF] Hitchman | Predictors of car smoking rules among smokers in France, Germany and the Netherlands[END_REF][START_REF] Mills | Home smoking bans among U.S. households with children and smokers. Opportunities for intervention[END_REF]. Il semble néanmoins raisonnable de penser que la législation prévoyant des zones libres de tabac dans les lieux publics a un effet bénéfique général sur la santé des enfants [START_REF] Faber | Smoke-free legislation and child health[END_REF].

CONCLUSION

Beaucoup de progrès ont été réalisés ces dernières années dans la compréhension des mécanismes intimes des maladies respiratoires de l'enfant. L'essor de la génétique, l'émergence de l'épigénétique illustre parfaitement l'importance de l'inné et de l'acquis. Chez l'enfant, notamment le petit, qui passe le plus clair de son temps à domicile, c'est la diminution de la pollution intérieure qu'il faut privilégier qu'elle soit environnementale (allergie, formaldéhyde) ou liée à la fumée de tabac. Malgré une accumulation de preuves sur les effets délétères multiorganes du tabagisme passif chez l'enfant, le problème demeure presque inchangé, quelle que soit la politique de santé publique. Peut-être faut-il concentrer nos efforts sur la grossesse car c'est bien à ce moment que la concentration délivrée à l'enfant est la plus forte, avec des conséquences à long terme impressionnantes. Un label maternité zéro tabac pourrait peut-être inciter les établissements à développer des politiques préventives pour peu que l'obtention de celui-ci conditionne des aides de l'état… Tableau I : valeur de référence de la cotinine dans les cheveux en fonction du statut de fumeur actif ou passif d'après Florescu A et coll [START_REF] Florescu | Reference values for hair cotinine as a biomarker of active and passive smoking in women of reproductive age, pregnant women, children, and neonates: systematic review and meta-analysis[END_REF]. On estime qu'à partir d'un taux de 0,2 ng/mg de cheveux l'enfant subit une exposition à la fumée de tabac.

  et de dosages placentaires et dans le sang du cordon effectué chez 20 fumeuses et 20 non fumeuses, ils ont pu démontrer la dérégulation d'un nombre très important de gènes, essentiellement impliqués dans le métabolisme xénobiotique, le stress oxydatif, l'immunité et la vascularisation. Pour Harding R et al (25), l'origine foetale des maladies pulmonaires de l'enfant ne fait pas de doute. Ils analysent les influences génétiques et environnementales, entraînant des altérations histologiques pulmonaires responsables d'anomalies de la fonction respiratoire. Leur résultats rejoignent ceux de Henderson AJ et al (26) sur la place centrale jouée par les expositions foetales dans la survenue d'un asthme chez l'enfant. Pour ces équipes, des modifications de l'expression de l'ADN liées à ces phénomènes toxiques pourraient être transmises de génération en génération, expliquant les risques accrus d'asthme chez les petits enfants de grands-mères (27) ayant fumé durant leur grossesse… C'est peut-être par le biais d'une intervention des récepteurs alpha nicotiniques que l'exposition à la nicotine prénatale altère la fonction respiratoire. Wongtrakool C et al (28) ont comparé les effets d'une exposition prénatale à la nicotine de deux séries de souris soumises à cette exposition, dont une est génétiquement dépourvue de récepteurs alpha nicotinique. Les altérations histologiques ne surviennent que chez celles qui sont porteuses de ces récepteurs. Rehan UK et al (29) pensent que l'effet du tabac pendant la grossesse est tardif. Il s'exprime essentiellement lors de la phase de maturation pulmonaire (Fig 2). Pour lui la nicotine entrave la communication entre l'épithélium et le mésenchyme en inhibant certaines signalisations et en stimulant le gène Wnt, favorisant la différenciation des lipofibroblastes en myofibroblastes.

  Dans une revue générale sur l'épigénétique et les influences prénatales sur l'asthme et les maladies allergiques, Martino D et al (31) rappellent l'importance du développement immunitaire et les modifications par l'environnement susceptibles d'orienter vers un profil particulier. L'enquète porte sur les agents infectieux, la nutrition, la pollution, et le tabac qui interviendrait par l'altération des schémas de méthylation de l'ADN de plusieurs gènes clés de ce développement. C'est ce type d'étude qu'ont effectué Halley KJ et coll (32), sur les facteurs de transcription RUNX (Runt-Relative Transcription Factor) qui jouent un rôle déterminant dans le développement du système immunitaire. L'analyse génomique a été réalisée chez des sujets asthmatiques. 17 des 100 polymorphismes (single nucleotid polymorphism) sont associés à une hyperréactivité bronchique à la métacholine. Cette association entre hyperréactivité bronchique à la métacholine et l'existence d'un polymorphisme est modifiée significativement par le tabagisme pendant la grossesse. Le tabac in utero accroît l'expression de RUNX1 au stade pseudoglandulaire. L'altération de l'expression de RUNX augmente le risque d'asthme chez l'enfant exposé au tabac durant la grossesse. Brooks CC et al viennent de démontrer récemment (33) que des variations génomiques dans le gène NAT modifient les risques d'asthme chez les enfants soumis au tabagisme passif.

  Hansen K et al[START_REF] Hansen | Early exposure to secondhand tobacco smoke and the development of allergic diseases in 4 year old children in Malmö, Sweden[END_REF] ont analysé les habitudes tabagiques chez 4 278 enfants examinés pour les bilans de 4 ans. Si au moins un parent fume, il y a une augmentation de 2 à 4 du risque d'asthme ou d'allergie. Cet effet est majoré en cas d'antécédents familiaux d'allergie. Tanaka K et al (38) retrouvent cette même association chez 1 951 enfants de moins de 3 ans au Japon avec une prévalence d'eczéma à 17 % augmentée en cas d'IPFT. Pour Ruskamp J et al (46), c'est surtout le tabagisme in utero qui est responsable de cette augmentation. Ils ont analysé une cohorte de 2 863 enfants dont 914 ont eu un prélèvement d'IgE totales à la naissance. Ce sont les enfants qui ont des taux d'IgE cordonales les plus élevés qui ont eu une dermatite atopique et ont été exposés au tabac durant la grossesse. La modification de la réponse immunitaire normale induite par le tabagisme passif pourrait expliquer ces constatations (Fig 3). Cet effet est démontré chez l'animal. L'IPFT chez la souris provoque une polarisation TH2, augmente la synthèse des IgE totales, de l'IL4 et de l'IL13

  . L'utilisation d'un purificateur d'air au domicile des parents fumeurs visant à améliorer la qualité de l'air intérieur est une piste potentielle. Butz AM et al (58) nous font part de leur expérience dans ce domaine en comparant 126 enfants vivant avec un fumeur répartis en trois groupes : le premier (n=41) bénéficie de l'installation d'un purificateur d'air, le second (n=41) d'un même purificateur d'air et d'un éducateur à la santé, enfin le troisième n'a aucune aide instrumentale et médicale. Il existe une diminution significative de la concentration en petites particules (PMM=2.5-10) mais pas en cotinine. Il y a une augmentation significative de jours sans symptôme dans les deux groupes bénéficiant d'un purificateur d'air, mais ceci n'est pas suffisant pour prévenir les exacerbations. Il faut indiscutablement renforcer l'information des parents pour limiter l'inhalation passive de la fumée de tabac chez les nourrissons. Mills LM et al (59) ont analysé l'exposition à la fumée de tabac chez des enfants de 1 à 5 ans dont les mères fument à la maison. Ils ont réalisé dans 54 maisons des mesures de concentration en particules fines et ont dosé la cotinine salivaire. Dans 89 % des maisons, la concentration (PMM=2.5) dépasse les niveaux autorisés par les autorités de santé entre 18 h et minuit. Ce sont les enfants plus petits qui ont les concentrations de cotinine les plus élevés, avec des valeurs moyennes à 2.35 ng/ml. Il semble que les interventions à domicile par des éducateurs à la santé soient très difficiles à mettre en place, et surtout peu contributives dans cette lutte contre le tabagisme passif. Ainsi Maas T et al (60) ont proposé, chez des enfants génétiquement prédisposés, une stratégie préventive visant à réduire l'exposition allergique, promouvoir l'allaitement maternel et diminuer l'IPFT. 476 enfants ont été inclus durant la grossesse dont 222 ont bénéficié d'un programme interventionnel contre 221 contrôles. Ils ont obtenu une diminution de l'exposition aux acariens, aux phanères animaux et une augmentation de l'allaitement maternel, mais sans réduction significative de l'exposition à la fumée de tabac, et donc aucune influence sur la prévalence de l'asthme à 6 ans. Ortega G et al (61) proposent d'intégrer un programme de prévention du tabagisme passif chez les nourrissons de moins de 18 mois, en utilisant les visites systématiques du pédiatre et en faisant une éducation à la santé régulière pour expliquer les méfaits du IPTF. L'efficacité d'un tel programme sera analysée sur un panel représentatif de nourrissons pour lesquels on aura mesuré les concentrations de cotinine dans les cheveux au départ et à 6 mois du programme. Il est difficile de savoir si l'instauration des politiques antitabac dans la plupart des pays de la communauté européenne a modifié les habitudes tabagiques des parents à domicile. Pour Holliday JC et al (62), qui ont réalisé une étude au Pays de Galle après instauration des lois antitabac, le bénéfice est certain pour l'exposition dans les lieux publics, mais sans changement notable sur l'exposition à la maison. Callinan JE et al (63) ont recensé 50 articles sur les répercussions des lois anti-tabac. Ils démontrent une diminution significative de l'IPTF sur les lieux de travail, les restaurants et les espaces publics, mais sans impact significatif dans les voitures et à la maison. C'est l'impression générale soulignée par d'autres publications sur cette question des habitudes tabagiques et de la législation anti-tabac

Légendes Figure 3

 3 Figure 3 : effets immunologiques du tabac modifié d'après Strzelak A et al (44)

Tableau I : valeur de référence de la cotinine dans les cheveux en fonction du statut de fumeur actif ou passif d'après Florescu A et coll [START_REF] Florescu | Reference values for hair cotinine as a biomarker of active and passive smoking in women of reproductive age, pregnant women, children, and neonates: systematic review and meta-analysis[END_REF]. On estime qu'à partir d'un taux de 0,2 ng/mg de cheveux l'enfant subit une exposition à la fumée de tabac.