Abstract
Background
Lifestyle interventions have been proposed to be the first-line treatment for polycystic ovarian syndrome (PCOS), but our knowledge of PCOS-related lifestyle factors is still limited. This study aimed to explore PCOS-related lifestyle factors in reproductive-age women in China.
Methods
A case-control study was carried out in Shandong, China, from June to October 2014. 350 PCOS-related infertile women were recruited as cases, while 308 women who were seeking the treatment of fallopian tube obstruction or assisted reproduction due to male infertility were recruited as controls. Several specific lifestyle and behavioral factors associated with EDC exposure were examined. Multivariate logistic regression analysis was used to estimate the odds ratios (ORs) and 95% confidence intervals (CI).
Results
There were no differences in socio-demographic characteristics, smoking, and alcohol consumption between the cases and controls. PCOS women had significantly more obesity than the controls (P < 0.01). After controlling for potential confounders, using foam or plastic cups at home (daily vs. never: adjusted odds ratio [aOR] 2.6, 95% confidence interval [CI] 1.4–4.5), using foam or plastic tableware at home (occasionally vs. never: aOR 1.7, 95% CI 1.2–2.5), eating melons and fruits without pericarp (for occasionally vs. always/often: aOR 1.6, 95% CI 1.0–2.5), drinking tap water vs. spring water/bottled water (aOR 1.5, 95% CI 1.1–2.2), cooking (daily vs. ≤ 1 time/week: aOR 1.8, 95% CI 1.2–2.8), contacting liquid detergent (1.5 to 3 h/week vs. < 1.5 h/week, aOR 2.5, 95% CI 1.3–4.9), and contacting soap or shampoo (3–6 vs. < 3 h/week, aOR 2.1, 95% CI 1.2–3.8) were significantly associated with PCOS. The association between mild cooking oil fumes and PCOS risk was attenuated after adjustment, but it remained borderline significant (aOR 1.4, 95% CI 0.97–1.9).
Conclusions
Our study suggests that PCOS may be associated with certain lifestyle factors. Future prospective studies are needed to confirm our findings.
Supplementary Information
The online version contains supplementary material available at 10.1186/s13048-026-02034-9.
Keywords: Lifestyle factors, Behavior, Endocrine disruptors, Polycystic ovary syndrome
Introduction
Polycystic ovary syndrome (PCOS) is one of the most prevalent endocrine abnormalities in women of reproductive age. A recent systematic review reported that the prevalence ranges from 5% to 18% worldwide according to the 2003 Rotterdam criteria [1]. Current estimates using the Rotterdam criteria indicate a PCOS prevalence of 7.8% among Chinese women aged 20–49 in 2020, a 65% increase over the past decade. Notably, the rate exceeds 14% among women aged 20–30 [2]. This syndrome is often associated with multiple health conditions, such as metabolic disturbance, cardiovascular diseases, reproductive abnormalities, infertility, and psychological problems [3, 4]. Maternal PCOS has also been linked to an increased risk of perinatal and long-term adverse outcomes in the offspring [5, 6].
Despite its prevalence, the etiology of PCOS remains unclear. Lifestyle factors have been associated with PCOS. Recent research has reviewed the current knowledge about major modifiable risk factors in PCOS development [7]. Women with PCOS were more likely to have inappropriate dietary composition, less physical activity, inadequate sleep hygiene, elevated stress or depression, as well as higher incidences of smoking and alcohol use compared to healthy women [7, 8]. Lifestyle and behavioral interventions such as managing weight, developing healthy dietary habits (e.g., lower calorie intake), and keeping physical exercise, have been recommended to improve reproductive functions, endocrine parameters, cardiometabolic profiles, and psychological health in PCOS women [9]. It was even considered as the first-line therapy for PCOS [10]. However, these interventions may not address all underlying lifestyle factors that contribute to the development and long-term persistence of PCOS [9].
Accumulating evidence indicates a connection between endocrine-disrupting chemicals (EDCs) and the pathogenesis and/or more severe symptoms of PCOS [11]. EDCs are exogenous compounds comprising a wide range of natural and synthetic chemicals such as bisphenol A (BPA), some pesticides, triclosan (TCS), and polycyclic aromatic hydrocarbons (PAHs) [12, 13]. Humans can be widely exposed to EDCs through dietary ingestion, absorption through the skin and mucous membranes, and inhalation [14]. Mounting evidence demonstrated the adverse effects of EDCs on the endocrine system and reproductive functions [14]. These exogenous compounds may also interfere with metabolic homeostasis, impair insulin sensitivity, induce changes in epigenetic modifications, and exert a regulatory effect on genetic susceptibility [14].
Lifestyle modifications and behavioral interventions addressing EDCs exposure will undoubtedly play an important role in comprehensive PCOS management. The current key recommendations [15] for the general population include avoiding plastic food/beverage containers by using glass, ceramic, or stainless steel ceramic alternatives; reducing canned food consumption, as the internal coatings of metal cans may leach BPA; prioritizing organic, home-cooked meals instead of processed/packaged options that may contain bisphenols and phthalates; selecting natural cleaners like vinegar and baking soda rather than chemical ones; choosing personal care items formulated without parabens, phthalates, or triclosan; and improving indoor air quality through ventilation to reduce airborne EDCs levels.
Most previous studies primarily focus on detecting EDC biomarkers, rather than establishing a clear link between the specific lifestyle behaviors that may lead to EDC exposure and PCOS. This study aimed to explore the association between lifestyle-mediated environmental exposures (i.e., various household lifestyle factors in China that may contribute to EDCs exposure) and PCOS among reproductive-age Chinese women-specifically including the use of foamed cups and tableware that often contain BPA, contact with soap, shampoo or liquid detergent containing TCS, habits of eating melons and fruits with pericarp and/or eating vegetables without soaking which may contain pesticide residues, consumption of drinking water which may contain pesticides or other chemicals, and cooking-related factors, such as oil fumes and the combustion process of fuels used, which may release harmful compositions such as polycyclic aromatic hydrocarbons (PAHs). The findings may provide targeted lifestyle intervention recommendations for PCOS in the Chinese population.
Materials and methods
Study design and patients
From June to October 2014, a case-control study was conducted at the Centre for Reproductive Medicine, Shandong University, Shandong, China. All potential subjects were couples seeking medical care for infertility (couples had regular unprotected intercourse within the past year, but had failed to conceive). Both females and their partners had undergone a complete workup for the diagnosis of infertility.
We included women into the case group with PCOS-related infertility if they were married, aged 20–40 years, diagnosed as PCOS based on the Rotterdam criteria, namely meeting two or three of the following item: (1) oligo-ovulation or anovulation; (2) biochemical hyperandrogenism and/or clinical hyperandrogenism while other disorders related to androgen excess excluded; (3) polycystic ovaries [16]; had no tubal obstruction or other specific infertility factors; and their husbands had normal fertility. The control group included women who were married, 20–40 years old, and came to the center for the treatment of fallopian tube obstruction or male infertility. A total of 350 women who had PCOS-related infertility were recruited as cases, and 308 women were included as controls. The method for sample size calculation was described in the supplementary file. Patients with PCOS-related infertility in the case group were diagnosed when they attended infertility clinics for treatment. Infertility is defined as the inability of couples to achieve a clinical pregnancy after 12 consecutive months of regular sexual intercourse without contraception [17].
Interviews
All cases and controls were interviewed by trained staff. Information collected was the socio-demographic characteristics, menstrual and reproductive history, work and lifestyle factors, personal medical history and family history. The collection of lifestyle factors was based on lifestyle patterns associated with environmental pollutant exposure previously reported in the literature, and it also took into account the prevalence of these behaviors among the Chinese population. The participants and the interviewer were unaware of the hypothesis of the present study, which examined the association between lifestyle factors and PCOS. This study was approved by the Institutional Review Board at Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. A written consent form was signed by all participants.
Exposure information
Women’s occupations were categorized into five groups: office and service workers/soldiers/teachers/doctors/students (reference group); farmers/herdsmen/fishermen; engineers/chemical factory workers/clothing or food processing workers; unemployed; and others/unknown. The frequency of using foam or plastic cups at home and the frequency of using plastic tableware were categorized as: never (reference), occasionally, most of the time, daily, and unknown. The categorization of other exposures were as follows: eating melons and fruits without pericarp (always/often [reference], occasionally, never, unknown), soaking vegetables before eating (yes [reference], no, unknown), source of drinking water (spring water/bottled water [reference], river water/well water, tap water, others/unknown), cooking frequency (rarely [reference], 2–3 times/week, 4–6 times/week, daily, unknown), type of cooking fuel (natural gas [reference], coal gas, others, unknown), cooking with coal gas (rarely cook [reference], 2–3 times/week, 4–6 times/week, daily), cooking with natural gas (rarely cook [reference], 2–3 times/week, 4–6 times/week, daily), cooking oil fumes (COFs: no [reference], mild, heavy), cooking with no COFs (rarely cook [reference], 2–3 times/week, 4–6 times/week, and daily), cooking with mild COFs (rarely cook [reference], 2–3 times/week, 4–6 times/week, and daily). Infrequent cooking was defined as cooking ≤ 1 time per week, regardless of whether there were COFs or the type of cooking fuel (CF) used. Contacting soap or shampoo (≤ 3 h/week [reference], 3–6 h/week, > 6 h/week, unknown), contacting liquid detergent (≤ 1.5 h/week [reference], 1.5–3 h/week, > 3 h/week, unknown), using air freshener (never [reference], occasionally, most of the time, daily, unknown), average outdoor time per week (< 10 h [reference], 10–20 h, > 20 h, unknown), average sedentary time per day (< 4 h [reference], 4–8 h, > 8 h, unknown) and residential traffic flow (small [reference], medium, large, unknown).
Other covariates
Sociodemographic characteristics included female age (≤ 25, 25–30 [reference], 30–35, > 35 years and unknown), female educational level (≤ 6, 6–9 [reference], 10–12, 13–16, ≥ 17 years and unknown), female body mass index (BMI, < 18.5, 18.5–25 [reference], and ≥ 25 kg/m2, unknown), annual income (< 30,000 [reference], 30,000–50,000, 50,000–100,000, ≥ 100,000 RMB/person, unknown).
Statistical analysis
Differences in socio-demographic characteristics (all categorical) between cases and controls were compared using Chi-square tests. Multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between exposure variables and PCOS, controlling for potential confounders such as age, women’s educational level, household income, and BMI. In the primary analysis, univariate and multivariate logistic regression analyses were repeated after excluding the missing data for exposure variables. In the sensitivity analysis, missing data for all exposure variables and covariates were imputed using multiple imputation by fully conditional specification (MI-FCS) [18, 19]. The results were pooled by concatenating ten imputed datasets that had no missing data. All the analyses were conducted using SAS version 9.4.
Results
Table 1 shows that women with PCOS had a higher proportion of obesity than the controls. There were no significant differences in socio-demographic characteristics, smoking, and alcohol consumption between the cases and controls.
Table 1.
Demographic characteristics in PCOS cases and controls (n = 658)
| Characteristics | Cases n (%) |
Controls n (%) |
P |
|---|---|---|---|
| Female age (years) | 0.8 | ||
| ≤ 25 | 49 (14.0) | 51 (16.6) | |
| 25–30 | 190 (54.3) | 165 (53.6) | |
| 30–35 | 89 (25.4) | 72 (23.4) | |
| ≥ 35 | 18 (5.1) | 18 (5.8) | |
| Unknown | 4 (1.1) | 2 (0.7) | |
| Female educational level (years) | 0.9 | ||
| ≤ 6 | 28 (8.0) | 19 (6.2) | |
| 6–9 | 169 (48.3) | 152 (49.4) | |
| 10–12 | 87 (24.9) | 74 (24.0) | |
| 13–16 | 57 (16.3) | 53 (17.2) | |
| ≥ 17 | 3 (0.9) | 2 (0.7) | |
| Unknown | 6 (1.7) | 8 (2.6) | |
| Female occupation | 0.3 | ||
| Office and service workers/soldiers, teachers/doctors/students | 144 (41.1) | 138 (44.8) | |
| Farmers/herdsmen/fishermen | 31 (8.9) | 22 (7.1) | |
| Engineers/chemical factory workers/clothing or food processing workers | 36 (10.3) | 41 (13.3) | |
| Unemployed | 106 (30.3) | 88 (28.6) | |
| Unknown | 33 (9.4) | 19 (6.2) | |
| Annual income (RMB/person) | 0.1 | ||
| < 30,000 | 253 (72.3) | 197 (64.0) | |
| 30,000–50,000 | 53 (15.1) | 70 (22.7) | |
| 50,000–100,000 | 17 (4.9) | 20 (6.5) | |
| ≥ 100,000 | 8 (2.3) | 7 (2.3) | |
| Unknown | 19 (5.4) | 14 (4.5) | |
| *BMI (kg/m2) | < 0.0001 | ||
| < 18.5 | 13 (3.7) | 27 (8.8) | |
| 18.5–25 | 150 (42.9) | 170 (55.2) | |
| ≥ 25 | 163 (46.6) | 67 (21.7) | |
| Unknown | 24 (6.9) | 44 (14.3) | |
| Smoking status | 0.1 | ||
| Never | 326 (93.1) | 297 (96.4) | |
| Have quit smoking for half a year | 0 (0.00) | 1 (0.3) | |
| Occasionally or current smoking | 3 (0.9) | 0 (0.0) | |
| Unknown | 21 (6.0) | 10 (3.3) | |
| Alcohol consumption | 0.6 | ||
| Never | 307 (87.7) | 280 (90.9) | |
| Have quit drinking for a year | 7 (2.0) | 6 (2.0) | |
| Occasionally or regular drinking | 24 (6.9) | 14 (4.5) | |
| Unknown | 12 (3.4) | 8 (2.6) | |
*BMI body mass index
Table 2 shows that after adjusting for potential confounders, PCOS was significantly associated with using foam or plastic cups daily at home (adjusted odds ratio [aOR] 2.6, 95% confidence interval [CI] 1.4–4.5), using foam or plastic tableware occasionally at home (aOR 1.7, 95% CI 1.2–2.5), eating melons and fruits without pericarp (for occasionally vs. always/often: aOR 1.6, 95% CI 1.0–2.5), drinking tap water vs. spring water/bottled water (aOR 1.5, 95% CI 1.1–2.2), cooking (daily vs. ≤ 1 time/week, aOR 1.8, 95% CI 1.2–2.8). In the group of cooking with natural gas, cooking frequency was not associated with PCOS. Among women who cooked with coal gas, cooking every day increased the risk of PCOS (aOR 2.4, 95% CI 1.5–3.9) compared with those who rarely cooked. The association between mild COFs and PCOS risk was borderline significant (aOR 1.4, 95% CI 0.97–1.9). In women who reported cooking without COFs, cooking frequency was not associated with PCOS. However, among women who reported cooking with mild COFs, cooking every day was associated with an elevated risk of PCOS (aOR 2.3, 95% CI 1.4–3.7) compared with women who rarely cook. Contacting liquid detergent (1.5 to 3 h/week vs. < 1.5 h/week, aOR 2.5, 95% CI 1.3–4.9), and contacting soap or shampoo (3–6 vs. < 3 h/week, aOR 2.1, 95% CI 1.2–3.8) were associated with increased risks of PCOS. PCOS was not significantly associated with air freshener use, eating vegetables without soaking them, average daily sitting time, or occupation.
Table 2.
Association between lifestyle factors and PCOS
| Exposures | Cases n (%) |
Controls n (%) |
OR (95% CI) | aOR# (95% CI) |
|---|---|---|---|---|
| Female occupation (n = 606) | ||||
| Office and service workers, soldiers, teachers, doctors, students | 144 (45.4) | 138 (47.8) | Ref | Ref |
| Farmers, herdsmen and fishermen | 31 (9.8) | 22 (7.6) | 1.4 (0.7–2.4) | 1.1 (0.5–2.1) |
| Engineers, chemical factory workers, clothing or food processing workers | 36 (11.4) | 41 (14.2) | 0.8 (0.5–1.4) | 0.9 (0.5–1.7) |
| Unemployed | 106 (33.4) | 88 (30.4) | 1.2 (0.8–1.7) | 1.0 (0.7–1.6) |
| Using foam or plastic cups at home (n = 646) | ||||
| Never | 190 (55.4) | 193 (63.7) | Ref | Ref |
| Occasionally | 73 (21.3) | 63 (20.8) | 1.2 (0.8–1.7) | 1.1 (0.7–1.7) |
| Most of the time | 28 (8.2) | 26 (8.6) | 1.1 (0.6–1.9) | 1.2 (0.6–2.1) |
| Daily | 52 (15.2) | 21 (6.9) | 2.5 (1.5–4.3) | 2.6 (1.4–4.5) |
| Using foam or plastic tableware at home (n = 642) | ||||
| Never | 218 (64.7) | 228 (74.7) | Ref | Ref |
| Occasionally | 110 (32.6) | 68 (22.3) | 1.7 (1.2–2.4) | 1.7 (1.2–2.5) |
| Most of the time | 7 (2.1) | 6 (2.0) | 1.2 (0.4–3.7) | 1.2 (0.2–3.7) |
| Daily | 2 (0.6) | 3 (1.0) | 0.7 (0.1–4.2) | 0.4 (0.1–3.2) |
| Eating melons and fruits without pericarp (n = 646) | ||||
| Always/often | 68 (19.9) | 84 (27.5) | Ref | Ref |
| Occasionally | 136 (39.9) | 108 (35.4) | 1.6 (1.0–2.3) | 1.6 (1.0–2.5) |
| Never | 137 (40.2) | 113 (37.1) | 1.5 (1.0–2.3) | 1.5 (1.0–2.4) |
| Soaking vegetables before eating (n = 641) | ||||
| Yes | 246 (72.6) | 207 (68.5) | Ref | Ref |
| No | 93 (27.4) | 95 (31.5) | 0.8 (0.6–1.2) | 0.9 (0.6–1.2) |
| Drinking water (n = 644) | ||||
| Spring water/barrelled water | 92 (27.0) | 107 (35.3) | Ref | Ref |
| River water/well water | 40 (11.7) | 25 (8.3) | 1.8 (1.0–3.1) | 1.6 (0.9–3.1) |
| Tap water | 209 (61.3) | 171 (56.4) | 1.4 (1.0–1.9) | 1.5 (1.1–2.2) |
| Cooking (n = 637) | ||||
| ≤ 1 time/week | 77 (22.6) | 96 (32.4) | Ref | Ref |
| 2–3 times/week | 46 (13.5) | 38 (12.8) | 1.5 (0.9–2.5) | 1.6 (0.9–2.8) |
| 4–6 times/week | 29 (8.50) | 40 (13.5) | 0.9 (0.5–1.6) | 0.8 (0.5–1.5) |
| Daily | 189 (55.4) | 122 (41.2) | 1.9 (1.3–2.8) | 1.8 (1.2–2.8) |
| Source of fuels for cooking or heating (n = 624) | ||||
| Natural gas | 94 (27.7) | 94 (33.0) | Ref | Ref |
| Coal gas | 187 (55.2) | 127 (44.5) | 1.5 (1.0–2.1) | 1.4 (0.95–2.2) |
| Others* | 58 (17.1) | 64 (22.5) | 0.9 (0.6–1.4) | 0.9 (0.5–1.5) |
| Cooking using coal gas (n = 407) | ||||
| Rarely cook† | 77 (33.9) | 96 (53.3) | Ref | Ref |
| 2–3 times/week | 22 (9.7) | 17 (9.4) | 1.6 (0.8–3.3) | 1.7 (0.8–3.6) |
| 4–6 times/week | 20 (8.8) | 14 (7.8) | 1.8 (0.8–3.8) | 1.6 (0.7–3.4) |
| Daily | 108 (47.6) | 53 (29.4) | 2.5 (1.6–4.0) | 2.4 (1.5–3.9) |
| Cooking using natural gas (n = 315) | ||||
| Rarely cook† | 77 (53.9) | 96 (55.8) | Ref | Ref |
| 2–3 times/week | 15 (10.5) | 14 (8.1) | 1.3 (0.6–2.9) | 1.3 (0.6–3.2) |
| 4–6 times/week | 5 (3.5) | 17 (9.9) | 0.4 (0.1–1.0) | 0.4 (0.1–1.1) |
| Daily | 46 (32.2) | 45 (26.2) | 1.3 (0.8–2.1) | 1.1 (0.6–2.0) |
| Cooking oil fume (n = 612) | ||||
| None | 128 (38.6) | 132 (47.1) | Ref | Ref |
| Mild (not smoky) | 178 (53.6) | 131 (46.8) | 1.4 (1.0–2.0) | 1.4 (0.97–1.9) |
| Heavy (smoky) | 26 (7.8) | 17 (6.1) | 1.6 (0.8–3.0) | 1.5 (0.8–3.1) |
| Cooking with no oil fume (n = 341) | ||||
| Rarely cook† | 77 (48.1) | 96 (53.0) | Ref | Ref |
| 2–3 times/week | 14 (8.8) | 18 (9.9) | 1.0 (0.5–2.1) | 0.9 (0.4–2.1) |
| 4–6 times/week | 8 (5.0) | 19 (10.5) | 0.5 (0.2–1.3) | 0.5 (0.2–1.3) |
| Daily | 61 (38.1) | 48 (26.5) | 1.6 (1.0–2.6) | 1.5 (0.9–2.6) |
| Cooking with mild oil fume (n = 407) | ||||
| Rarely cook† | 77 (34.5) | 96 (52.2) | Ref | Ref |
| 2–3 times/week | 26 (11.7) | 16 (8.7) | 2.0 (1.0–4.0) | 2.3 (1.0–4.9) |
| 4–6 times/week | 17 (7.6) | 18 (9.8) | 1.2 (0.6–2.4) | 1.1 (0.5–2.4) |
| Daily | 103 (46.2) | 54 (29.4) | 2.4 (1.5–3.7) | 2.3 (1.4–3.7) |
| Contacting liquid detergent (n = 640) | ||||
| ≤ 1.5 h/week | 281 (82.7) | 275 (91.7) | Ref | Ref |
| 1.5–3 h/week | 36 (10.6) | 14 (4.7) | 2.5 (1.3–4.8) | 2.5 (1.3–4.9) |
| > 3 h/week | 23 (6.8) | 11 (3.7) | 2.0 (1.0–4.3) | 1.8 (0.8–3.9) |
| Contacting soap or shampoo (n = 641) | ||||
| ≤ 3 h/week | 290 (85.0) | 279 (93.0) | Ref | Ref |
| 3–6 h/week | 44 (12.9) | 20 (6.7) | 2.1 (1.2–3.7) | 2.1 (1.2–3.8) |
| > 6 h/week | 7 (2.1) | 1 (0.3) | 6.7 (0.8–55.0) | 4.9 (0.6–42.3) |
| Using air freshener (n = 646) | ||||
| Never | 291 (85.1) | 265 (87.2) | Ref | Ref |
| Occasionally | 49 (14.3) | 39 (12.8) | 1.1 (0.7–1.8) | 1.1 (0.7–1.8) |
| Most of the time | 1 (0.3) | 0 (0.0) | -- | -- |
| Daily | 1 (0.3) | 0 (0.0) | -- | -- |
| Average outdoor time per week (n = 633) | ||||
| < 10 h | 209 (63.0) | 199 (66.1) | Ref | Ref |
| 10–20 h | 69 (20.8) | 74 (24.6) | 0.9 (0.6–1.3) | 0.9 (0.6–1.3) |
| > 20 h | 54 (16.3) | 28 (9.3) | 1.8 (1.1–3.0) | 1.6 (0.9–2.7) |
| Average sitting time per day (n = 635) | ||||
| < 4 h | 120 (36.0) | 118 (39.1) | Ref | Ref |
| 4–8 h | 149 (44.7) | 120 (39.7) | 1.2 (0.9–1.7) | 1.2 (0.8–1.7) |
| > 8 h | 64 (19.2) | 64 (21.2) | 1.0 (0.6–1.5) | 0.9 (0.6–1.4) |
| Residential traffic flow (n = 646) | ||||
| Small | 97 (28.3) | 84 (27.7) | Ref | Ref |
| Medium | 165 (48.1) | 146 (48.2) | 1.0 (0.7–1.4) | 1.0 (0.7–1.5) |
| Large | 81 (23.6) | 73 (24.1) | 1.0 (0.6–1.5) | 0.9 (0.6–1.5) |
#Adjusted for female age (≤ 25, 25–30, 30–35, > 35, unknown), educational levels (≤ 6, 6–9, 10–12, 13–16, ≥ 17, unknown), annual income (< 30,000, 30,000–50,000, 50,000–100,000, ≥ 100,000 RMB, unknown), BMI (< 18.5, 18.5–25, ≥ 25 kg/m2, unknown)
†Rarely cook: cooking ≤ 1 time/week and regardless of whether there is cooking oil fumes and using what kind of cooking fuels
* Others: coal, wood, others
Supplementary Table 1 shows the results of the univariate and multivariate logistic regression analyses using complete case analysis. These results were consistent with those of the previous analyses. Supplementary Table 2 shows the results of associations between lifestyle factors and PCOS stratified by BMI. No distinct differences were observed across the groups, which may be attributable to the limited sample size.
Discussion
Our case-control study showed that PCOS was significantly associated with using foam or plastic cups or tableware, contacting soap, shampoo, or liquid detergent, eating melons and fruits with pericarp, and drinking tap water. We also found that COFs and daily cooking with coal gas were associated with increased odds of PCOS even after controlling for potential confounders. These factors have not been systematically studied in PCOS. Previous studies have suggested that these lifestyles are potential sources of exposure to endocrine-disrupting chemicals (EDCs), which have been linked to the development of PCOS [20, 21]. Therefore, our findings may be partly explained by exposure to EDCs.
In the present study, women with PCOS were more likely to use foam or plastic cups and tableware at home. This finding is consistent with a previous study conducted in Shandong, China, which reported that the frequency of plastic tableware usage was significantly higher in the PCOS oligo-anovulation (PCOS-OA) group than in the PCOS non-ovulatory dysfunction (PCOS-non-OD) group and the healthy control group (38.30% vs. 28.10% vs. 25.40%, P < 0.01) [22]. BPA has been extensively used in consumer products, such as food plastic packages, bottles and microwave containers [23]. BPA release from these products can be accelerated at high temperatures or in an acidic environment [24]. The average BPA concentrations in food in containers covered with plastic film far exceed the maximum acceptable daily intake (50 ug/kg body weight/day) [25]. Epidemiological evidence suggested that women with PCOS have higher serum, urinary, or follicular fluid concentrations of BPA than healthy women [20]. The animal experiment reported that neonatal BPA exposure leads to adulthood PCOS-like symptoms [21]. BPA plays a substantial role in disrupting the estrogen-androgen balance. It interacts with classical nuclear estrogen receptors and nonclassical membrane estrogen receptors [21] and stimulates theca cells in the ovary to produce androgen [26]. BPA can also increase androgen levels by displacing testosterone from sex hormone-binding globulin and inhibiting its catabolism [27, 28]. BPA has the ability to activate the pulse generator of GnRH, leading to an increase in LH secretion and a decrease in FSH secretion [29]. It was suggested that BPA might stimulate insulin production in pancreatic beta cells, thereby promoting lipid accumulation and aggravating ovarian dysfunction [21, 26]. Furthermore, long-term exposure to BPA has been linked to epigenetic modification [21]. All these possible pathways might have contributed to the increased risk of PCOS.
We also found that contacting soap, shampoo or liquid detergent more frequently was associated with a higher risk of PCOS. The cleaning household products were reported to have TCS [30], and TCS can be absorbed through skin contact [31]. There is evidence that TCS exerts significant estrogenic effects and weak androgenic effects, and might affect hormone homeostasis [20]. TCS may also affect the hypothalamus-pituitary-gonad axis, which not only increases GnRH secretion by enhancing GnRH expression but also disturbs the balance of estrogen and androgen by increasing aromatase gene expression [32]. Alternation in LH, FSH, and LH/FSH index, features of PCOS, were also documented in laboratory studies [32, 33].
In our study, women who ate melons and fruits with pericarp and drank tap water had higher odds of a PCOS diagnosis. Pesticides are widely used in agriculture at various stages to protect food crops from damage by pests or weeds [34]. A large number of pesticides have been detected in the peels of fruit and vegetables, as well as in surface water and groundwater [35, 36]; however, they showed much lower concentrations and detection rates in spring water or natural mineral water [37, 38]. Epidemiological studies have shown that serum concentrations of organochlorine pesticides (OCPs) in women with PCOS are significantly higher than those in the control group [39]. The underlying biological mechanism is not clear. It has been well documented that pesticides can interfere with estrogen and androgen pathways, acting as estrogen receptor agonists or androgen receptor antagonists [40]. A laboratory study also suggested that OCPs may disrupt the morphometry of GnRH and FSH cells and, consequently, alter circulating hormone levels [40, 41].
Our study suggests that during household cooking, oil fumes and emissions from fuel combustion may be risk factors for PCOS. Chinese-cooking styles are characterized by stir-frying, which can be a main source to increase the burden of household air pollution (HAP), which is a leading cause of disability-adjusted life years and death [42]. HAP from cooking sources was associated with adverse health conditions, such as cardiovascular diseases, diabetes, and pulmonary disease [43]. In addition, pollutants from fuel combustion during cooking prolonged the time to pregnancy and increased the risk of adverse pregnancy outcomes [44]. The aforementioned study conducted in Shandong specifically investigated the association between exposure to cooking oil fumes and PCOS ovulation status. However, its findings are inconsistent with ours, as it failed to identify significant differences in exposure frequency among the PCOS-OA, PCOS-non-OD, and healthy control groups [22]. A knowledge gap remains regarding cooking and the development of PCOS.
COFs and emissions from fuel combustion contain a diverse range of harmful compositions. Polycyclic aromatic hydrocarbons (PAHs) are a classic example [45]. The total annual emissions of PAHs for a Chinese restaurant are estimated at 2,038 kg, which is much higher than those for a Western restaurant (258 kg) and a Japanese restaurant (31.4 kg) [46]. Human data showed that women with PCOS had significantly higher serum levels of PAHs than healthy women [47]. In vivo animal model showed that PAHs exposure significantly reduced the number of fetal ovarian germ cells [48]. The aromatic hydrocarbon receptor pathway is a well-established target through which PAHs stimulate follicle apoptosis, and oocyte loss may result in premature ovarian failure, potentially leading to infertility [48, 49]. Besides endocrine disrupters, other pollutants released during cooking, such as particulate matter (PM), may also be associated with the increased incidence of PCOS. Previous studies showed that the average concentration of inhalable PM (PM2.5, 312.4 ug/m3) during cooking time was approximately 12-fold of that during non-cooking time (26.7 ug/m3) in a Chinese food stall [50]. Thus, the role of PAH and other endocrine disruptors deserves further investigation.
The main limitation of the current study is that the exposure information was self-reported by the women. It is possible that women who were diagnosed with PCOS might report exposures differently from the controls if they suspected that the exposure might affect their disease. But this may not be true in all instances [51–53]. Moreover, it was suggested that the observed association could not be due to recall bias unless participants’ beliefs changed after diagnosis [54]. For instance, as the harm of sedentary habits has been reported and physical exercise is advocated for PCOS management after diagnosis, the PCOS women may have had certain knowledge of the effects of sedentariness, which is likely to influence their answers to the question of “average sitting time per day. However, in our study, we observed comparable percentages of the average sitting time per day categorized as < 4 hours (36.0% vs. 39.1%), 4–8 hours (44.7% vs.39.7%), and > 8 hours (19.2% vs. 21.2%).
Second, the cases may tend to report more exposure if they know the study hypothesis [42]. But both the participants and the interviewer were unaware of the study’s hypothesis regarding the association between lifestyle factors and PCOS. Furthermore, our participants answered numerous lifestyle questions related to work, smoking and drinking status of individuals and their families, residential environment, and other factors in addition to household lifestyles. The questions on household and lifestyle factors were embedded among them. The associations between lifestyle factors and PCOS were unlikely to be due to recall or reporting bias.
A related, more specific methodological consideration was that our methodology did not include assessing major traditional lifestyle confounders, such as dietary intake and physical activity. In our initial case-control design, we chose not to collect these specific variables due to key methodological concerns. Unlike the household behaviors related to environmental exposures that are the focus of this study, behaviors like diet and exercise are well-established, modifiable risk factors for PCOS. Since our data were collected after diagnosis, reported behaviors could have been altered by the disease status itself (e.g., patients may change habits post-diagnosis). Measuring these factors retrospectively could thus introduce significant recall bias or reverse causality, where the disease influences the reporting of past behaviors rather than the behaviors causing the disease. Consequently, we prioritized assessing exposure-related household behaviors to test our primary hypothesis. Nevertheless, we acknowledge that these unmeasured traditional lifestyle factors remain potential sources of residual confounding.
It is also possible that after the diagnosis of PCOS, the cases had changed their behavior to avoid any suspected exposure. If this were true, our findings might have been underestimated. All these potential deficiencies call for future studies with more accurate assessments of exposures to corroborate our findings and uncover potential mechanisms.
Third, this study recruited all participants exclusively from infertility clinics, which introduces inherent selection bias. This sample cannot represent all women with PCOS; it solely represents women with PCOS-related infertility who are married and have actively sought clinical assistance. This study also did not include the following groups of women with PCOS: those with no fertility needs who are not in the preconception stage, unmarried women or those in non-heterosexual relationships, and those with occult symptoms or mild PCOS. Such limitations may limit the generalizability of the study’s findings.
Finally, the inability to clearly establish temporal associations is an inherent methodological limitation of the case-control design. Future studies should adopt multicenter, prospective designs with large sample sizes that encompass participants from diverse regions, ages, disease severities, and other relevant characteristics. This will enhance the external validity and generalizability of the findings.
Conclusions
Our study found that using foam or plastic cups or tableware, contact with soap, shampoo, or liquid detergent, eating melons and other fruits with pericarp, drinking tap water, daily cooking with coal gas, and COFs were associated with increased risks of PCOS. More research is warranted on this issue, as such findings may have important public health implications.
Supplementary Information
Acknowledgements
All participants are gratefully acknowledged.
Abbreviations
- aOR
adjusted odds ratio
- BMI
body mass index
- BPA
bisphenol A
- CIs
confidence intervals
- COFs
cooking oil fumes
- CF
cooking fuel
- EDCs
endocrine-disrupting chemicals
- HAP
household air pollution
- ORs
Odds ratios
- OCPs
organochlorine pesticides
- PCOS
polycystic ovarian syndrome
- PAHs
polycyclic aromatic hydrocarbons
- PM
particulate matter
- TCS
triclosan
Authors’ contributions
Xiaona Huo: Investigation, Conceptualization, Methodology, Software, Data curation, Writing - original draft. Han Liu: Investigation, Writing - Review & Editing. Min Nan: Data curation, Writing - Review & Editing. Jun Zhang: Project administration, Funding acquisition, Supervision, Visualization, Writing - Review & Editing.
Funding
This study was supported in part by the National Natural Science Foundation of China (No. 82574101) and the National Key Research and Development Program of China (2023YFC3905203).
Data availability
Data available on request from the corresponding author.
Declarations
Ethics approval and consent to participate
This study was conducted in accordance with the Declaration of Helsinki and approved by the Institutional Review Board at Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China (approval no. XHEC-C-2015-046). A written consent form was signed by all participants.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.Joham AE, Norman RJ, Stener-Victorin E, et al. Polycystic ovary syndrome. Lancet Diabetes Endocrinol. 2022;10(9):668–80. [DOI] [PubMed] [Google Scholar]
- 2.Yang R, Li Q, Zhou Z, et al. Changes in the prevalence of polycystic ovary syndrome in China over the past decade. Lancet Reg Health West Pac. 2022;25:100494. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Berni TR, Morgan CL, Rees DA. Women with polycystic ovary syndrome have an increased risk of major cardiovascular events: a population study. J Clin Endocrinol Metab. 2021;106(9):e3369–80. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Teede HJ, Tay CT, Laven J, et al. Recommendations from the 2023 international Evidence-based guideline for the assessment and management of polycystic ovary syndrome. Fertil Steril. 2023;120(4):767–93. [DOI] [PubMed] [Google Scholar]
- 5.Bahri Khomami M, Shorakae S, Hashemi S, et al. Systematic review and meta-analysis of pregnancy outcomes in women with polycystic ovary syndrome. Nat Commun. 2024;15(1):5591. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Stener-Victorin E, Teede H, Norman RJ, et al. Polycystic ovary syndrome. Nat Reviews Disease Primers. 2024;10(1):27. [DOI] [PubMed] [Google Scholar]
- 7.Capozzi A, Scambia G, Driul L, Vignali M, Lello S. Lifestyle and diet in PCOS. Minerva Obstet Gynecol. 2025;77(5):341–51. [DOI] [PubMed] [Google Scholar]
- 8.Kazemi M, Kim JY, Wan C, et al. Comparison of dietary and physical activity behaviors in women with and without polycystic ovary syndrome: a systematic review and meta-analysis of 39 471 women. Hum Reprod Update. 2022;28(6):910–55. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Gautam R, Maan P, Jyoti A, Kumar A, Malhotra N, Arora T. The role of lifestyle interventions in PCOS management: a systematic review. Nutrients. 2025;17(2):310. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Liao C, Wang T, Cui L, Zhou Q, Duan S, Jiang G. Changes in synaptic transmission, calcium current, and neurite growth by perfluorinated compounds are dependent on the chain length and functional group. Environ Sci Technol. 2009;43(6):2099–104. [DOI] [PubMed] [Google Scholar]
- 11.Lemogne Robert A, Oliveira Torres E, Jota Baptista C. Effects of endocrine disruptive chemicals (EDCs) and therapeutic approaches to the polycystic ovary syndrome (PCOS): A current state-of-the-art. Environ Toxicol Pharmacol. 2025;120:104842. [DOI] [PubMed] [Google Scholar]
- 12.Xu L, Hu Y, Zhu Q, Liao C, Jiang G. Several typical endocrine-disrupting chemicals in human urine from general population in china: regional and demographic-related differences in exposure risk. J Hazard Mater. 2022;424(Pt B):127489. [DOI] [PubMed] [Google Scholar]
- 13.Kahn LG, Philippat C, Nakayama SF, Slama R, Trasande L. Endocrine-disrupting chemicals: implications for human health. Lancet Diabetes Endocrinol. 2020;8(8):703–18. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Yilmaz B, Terekeci H, Sandal S, Kelestimur F. Endocrine disrupting chemicals: exposure, effects on human health, mechanism of action, models for testing and strategies for prevention. Rev Endocr Metab Disord. 2020;21(1):127–47. [DOI] [PubMed] [Google Scholar]
- 15.Martin L, Zhang Y, First O, et al. Lifestyle interventions to reduce endocrine-disrupting phthalate and phenol exposures among reproductive age men and women: A review and future steps. Environ Int. 2022;170:107576. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertility and sterility. 2004;81(1):19–25. [DOI] [PubMed]
- 17.Zegers-Hochschild F, Adamson GD, de Mouzon J, et al. International Committee for Monitoring Assisted Reproductive Technology (ICMART) and the World Health Organization (WHO) revised glossary of ART terminology, 2009. Fertility and sterility. 2009;92(5):1520–1524. [DOI] [PubMed]
- 18.Liu Y, De A. Multiple imputation by fully conditional specification for dealing with missing data in a large epidemiologic study. Int J Stat Med Res. 2015;4(3):287–95. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Lee KJ, Carlin JB. Multiple imputation for missing data: fully conditional specification versus multivariate normal imputation. Am J Epidemiol. 2010;171(5):624–32. [DOI] [PubMed] [Google Scholar]
- 20.Srnovršnik T, Virant-Klun I, Pinter B. Polycystic ovary syndrome and endocrine disruptors (Bisphenols, Parabens, and Triclosan)-A systematic review. Life (Basel). 2023;13(1):138. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Urbanetz L, Junior JMS, Maciel GAR, Simões RDS, Baracat MCP, Baracat EC. Does bisphenol A (BPA) participates in the pathogenesis of polycystic ovary syndrome (PCOS)? Clin (Sao Paulo). 2023;78:100310. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Zhang B, Zhou W, Shi Y, Zhang J, Cui L, Chen ZJ. Lifestyle and environmental contributions to ovulatory dysfunction in women of polycystic ovary syndrome. BMC Endocr Disord. 2020;20(1):19. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Besaratinia A. The state of research and weight of evidence on the epigenetic effects of bisphenol A. Int J Mol Sci. 2023;24(9):7951. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.Khalili Sadrabad E, Hashemi SA, Nadjarzadeh A, Askari E, Akrami Mohajeri F, Ramroudi F. Bisphenol A release from food and beverage containers - A review. Food Sci Nutr. 2023;11(7):3718–28. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Sungur S, Koroglu M, Ozkan A. Determination of bisphenol a migrating from canned food and beverages in markets. Food Chem. 2014;142:87–91. [DOI] [PubMed] [Google Scholar]
- 26.Rutkowska A, Rachon D. Bisphenol A (BPA) and its potential role in the pathogenesis of the polycystic ovary syndrome (PCOS). Gynecol Endocrinology: Official J Int Soc Gynecol Endocrinol. 2014;30(4):260–5. [DOI] [PubMed] [Google Scholar]
- 27.Hanioka N, Jinno H, Nishimura T, Ando M. Suppression of male-specific cytochrome P450 isoforms by bisphenol A in rat liver. Arch Toxicol. 1998;72(7):387–94. [DOI] [PubMed] [Google Scholar]
- 28.Dechaud H, Ravard C, Claustrat F, de la Perriere AB, Pugeat M. Xenoestrogen interaction with human sex hormone-binding Globulin (hSHBG). Steroids. 1999;64(5):328–34. [DOI] [PubMed] [Google Scholar]
- 29.Fernandez M, Bourguignon N, Lux-Lantos V, Libertun C. Neonatal exposure to bisphenol a and reproductive and endocrine alterations resembling the polycystic ovarian syndrome in adult rats. Environ Health Perspect. 2010;118(9):1217–22. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 30.Wang Y, Li G, Zhu Q, Liao C. Occurrence of parabens, triclosan and triclocarban in paired human urine and indoor dust from two typical cities in China and its implications for human exposure. Sci Total Environ. 2021;786:147485. [DOI] [PubMed] [Google Scholar]
- 31.Weatherly LM, Gosse JA. Triclosan exposure, transformation, and human health effects. J Toxicol Environ Health B Crit Rev. 2017;20(8):447–69. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32.Wang F, Guo X, Chen W, Sun Y, Fan C. Effects of triclosan on hormones and reproductive axis in female yellow river carp (Cyprinus carpio): potential mechanisms underlying Estrogen effect. Toxicol Appl Pharmcol. 2017;336:49–54. [DOI] [PubMed] [Google Scholar]
- 33.Ahsan N, Ullah H, Ullah W, Jahan S. Comparative effects of bisphenol S and bisphenol A on the development of female reproductive system in rats; a neonatal exposure study. Chemosphere. 2018;197:336–43. [DOI] [PubMed] [Google Scholar]
- 34.Wahab S, Muzammil K, Nasir N, et al. Advancement and new trends in analysis of pesticide residues in food: a comprehensive review. Plants (Basel). 2022;11(9):1106. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Si WS, Wang SY, Zhang YD, Kong C, Bai B. Pesticides and risk assessment in Shanghai fruit and Raw eaten vegetables. Food Addit Contam Part B Surveill. 2021;14(4):245–55. [DOI] [PubMed] [Google Scholar]
- 36.Syafrudin M, Kristanti RA, Yuniarto A, et al. Pesticides in drinking Water-A review. Int J Environ Res Public Health. 2021;18(2):468. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Le Coadou L, Le Menach K, Labadie P, et al. Quality survey of natural mineral water and spring water sold in france: monitoring of hormones, pharmaceuticals, pesticides, perfluoroalkyl substances, phthalates, and alkylphenols at the ultra-trace level. Sci Total Environ. 2017;603–604:651–62. [DOI] [PubMed] [Google Scholar]
- 38.Lapworth DJ, Baran N, Stuart ME, Manamsa K, Talbot J. Persistent and emerging micro-organic contaminants in chalk groundwater of England and France. Environ Pollut. 2015;203:214–25. [DOI] [PubMed] [Google Scholar]
- 39.Garg R, Goswami B, Singh K, et al. Association of organochlorine pesticide exposure as endocrine disruptors with polycystic ovarian syndrome in North India. J Midlife Health. 2025;16(2):201–7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.Yin S, Yang W, Lin F, et al. Polycystic ovary syndrome and organochlorine pesticides: exploring potential links and mechanisms. Front Reprod Health. 2025;7:1563414. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Piazza Y, Pandolfi M, Da Cuna R, Genovese G, Lo Nostro F. Endosulfan affects GnRH cells in sexually differentiated juveniles of the perciform Cichlasoma dimerus. Ecotoxicol Environ Saf. 2015;116:150–9. [DOI] [PubMed] [Google Scholar]
- 42.Khan MN, Mofizul Islam CZBN, Islam M, Rahman MR. Household air pollution from cooking and risk of adverse health and birth outcomes in bangladesh: a nationwide population-based study. Environ Health: Global Access Sci Source. 2017;16(1):57. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 43.Global regional, national burden of household air pollution. 1990–2021: a systematic analysis for the global burden of disease study 2021. Lancet. 2025;405(10485):1167–81. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 44.Shine S, Tamirie M, Kumie A, et al. Pregnant women’s perception on the health effects of household air pollution in rural Butajira, ethiopia: a phenomenological qualitative study. BMC Public Health. 2023;23(1):1636. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Lin C, Huang RJ, Duan J, Zhong H, Xu W. Polycyclic aromatic hydrocarbons from cooking emissions. Sci Total Environ. 2022;818:151700. [DOI] [PubMed] [Google Scholar]
- 46.Li CT, Lin YC, Lee WJ, Tsai PJ. Emission of polycyclic aromatic hydrocarbons and their carcinogenic potencies from cooking sources to the urban atmosphere. Environ Health Perspect. 2003;111(4):483–7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 47.Yang Q, Zhao Y, Qiu X, Zhang C, Li R, Qiao J. Association of serum levels of typical organic pollutants with polycystic ovary syndrome (PCOS): a case-control study. Hum Reprod. 2015;30(8):1964–73. [DOI] [PubMed] [Google Scholar]
- 48.Stefansdottir A, Marečková M, Matkovic M, Allen CM, Spears N. In vitro exposure to benzo[a]pyrene damages the developing mouse ovary. Reprod Fertil. 2023;4(2):e220071. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 49.Matikainen T, Perez GI, Jurisicova A, et al. Aromatic hydrocarbon receptor-driven Bax gene expression is required for premature ovarian failure caused by biohazardous environmental chemicals. Nat Genet. 2001;28(4):355–60. [DOI] [PubMed] [Google Scholar]
- 50.See SW, Balasubramanian R. Risk assessment of exposure to indoor aerosols associated with Chinese cooking. Environ Res. 2006;102(2):197–204. [DOI] [PubMed] [Google Scholar]
- 51.Cockburn M, Hamilton A, Mack T. Recall bias in self-reported melanoma risk factors. Am J Epidemiol. 2001;153(10):1021–6. [DOI] [PubMed] [Google Scholar]
- 52.Shaw GM, Swan SH, Harris JA, Malcoe LH. Maternal water consumption during pregnancy and congenital cardiac anomalies. Epidemiology. 1990;1(3):206–11. [DOI] [PubMed] [Google Scholar]
- 53.Lizama N, Heyworth J, Thomson A, Slevin T, Fritschi L. Self-reported shift work, recall bias, and belief about disease causation in a case-control study of breast cancer. Cancer Epidemiol. 2017;50(Pt A):9–15. [DOI] [PubMed] [Google Scholar]
- 54.Zota AR, Aschengrau A, Rudel RA, Brody JG. Self-reported chemicals exposure, beliefs about disease causation, and risk of breast cancer in the cape Cod breast cancer and environment study: a case-control study. Environ Health: Global Access Sci Source. 2010;9:40. [DOI] [PMC free article] [PubMed] [Google Scholar]
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Supplementary Materials
Data Availability Statement
Data available on request from the corresponding author.
