Association between smoke exposure and headache among U.S adolescents: a cross-sectional study from the NHANES 1999-2004

doi:10.21203/rs.3.rs-4334509/v1

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Association between smoke exposure and headache among U.S adolescents: a cross-sectional study from the NHANES 1999-2004

https://doi.org/10.21203/rs.3.rs-4334509/v1

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Background

Headaches are increasingly common among adolescents, with smoking considered a contributing risk factor. Cotinine, a nicotine metabolite, serves as an objective measure of smoke exposure. However, there is limited clinical data on the relationship between serum cotinine levels and headaches in adolescents.

Methods

A cross-sectional study design was applied, and participants aged 12 to 19 years from the National Health and Nutrition Examination Survey (NHANES) 1999–2004 were included in the analysis. Headache data were obtained through interviews and self-reports. Smoke exposure levels were categorized as unexposed, low secondhand smoke (SHS) exposure, high SHS exposure, and active smoking groups based on serum cotinine levels. The main analyses employed weighted multivariable logistic regression models, accounting for the complex multi-stage sampling design of NHANES. Additionally, a restricted cubic spline model was used to investigate the non-linear relationship between serum cotinine levels and headache. Furthermore, a subgroup analysis was conducted.

Results

The analysis included 5590 adolescents aged 12 to 19 years, among whom 1442 (24.99%) experienced headaches. After adjusting for all covariates, a positive association was found between log₂-transformed serum cotinine and headaches (odds ratio, R=1.04 (1.01, 1.07), P = 0.008). Adolescents with high SHS exposure (serum cotinine levels of 0.316 –10 ng/ml) and those in the active smoking group (serum cotinine≥10 ng/ml) had a higher risk of experiencing headaches compared to the unexposed group (serum cotinine < 0.05 ng/ml) [OR = 1.42 (1.07, 1.90), OR = 1.55 (1.06, 2.27), P for trend = 0.006]. A linear dose-response relationship was observed between log₂-transformed serum cotinine and the risk of headaches (P non-linearity > 0.05). Subgroup analysis revealed that the positive associations remained regardless of gender and varied depending on age and central obesity.

Conclusion

In conclusion, higher smoke exposure, as measured by elevated cotinine levels, was significantly associated with an increased risk of headaches among adolescents. Future research should focus on identifying effective strategies to eliminate smoke exposure and discourage tobacco use in adolescents prevent in adolescents to prevent headaches.

NHANES

Adolescents

Smoke exposure

Headache

Secondhand smoke

Headaches are a prevalent and debilitating issue among adolescents, with an estimated 75% of children reporting significant headaches by the age of 15 years^{[1, 2]}. The prevalence of frequent or severe headache in prepubertal children is 4–5% whereas estimates for post-pubertal age are much higher, ranging from 9–29% for frequent or severe headache^{[3, 4]}. Regular headaches in adolescents lead to reduced quality of life, limitations in social, educational, and professional spheres, and an increased risk of developing psychiatric disorders such as depression and anxiety, as well as other somatic symptoms like abdominal pain^[5–7]. There are numerous factors that contribute to the risk of developing headaches in adolescents, with several studies identifying cigarette smoking as an environmental risk factor for headaches in this population^[8].

Smoke exposure, which includes both active smoking and SHS, is a significant contemporary environmental pollution issue and an independent risk factor for various health conditions. Cigarette smoke contains numerous toxic and harmful substances, such as nicotine, heavy metals (such as arsenic, cadmium, and lead), and tar, which may affect headache activity^[9]. Environmental smoke exposure has been linked to numerous adverse health outcomes, including frequent and severe asthma attacks, respiratory infections, ear infections in children^{[10, 11]}. Due to the susceptibility of children and adolescents to the effects of passive smoking on their immature respiratory and immune systems, they may be more prone to experiencing headaches when exposed to secondhand smoke. However, the association between smoke exposure and headaches in adolescents has not yet been studied in a representative sample in the United States.

In previous studies on the association between smoke exposure and headaches in adolescents, researchers often used self-reported smoking status to assess risk^{[12, 13]}. However, this measure is prone to underestimation and reporting biases^[14]. Moreover, variations in smoking behavior that can affect pathophysiology, such as inhalation depth, are difficult to capture with questionnaires. Cotinine, a metabolite of nicotine, is considered a reliable marker of smoke exposure (both active and passive smoking) over the past 3 days and has greater sensitivity and specificity than other biomarkers.

Several studies using NHANES have shown that good reliability of self-reported current smoking status and cotinine levels, while estimating passive smoking exposure in non-smokers is more challenging^{[15, 16]}. Additionally, there is low concordance between biologic assessments of smoking status and self-reports among adolescents, as smoking may be more sporadic in this age group, and socially desired responses may lead to underreporting of current or passive smoking.

The relationship between active and passive smoking and headaches among adolescents has not been clearly established. We conducted a population-based investigation to determine the association between cotinine verification of smoking exposure and headaches among adolescents in the US NHANES. Our findings offer epidemiological evidence to further explore the connections between tobacco smoke exposure and headaches.

2.1. Study population

NHANES is a comprehensive cross-sectional survey carried out in the United States to furnish impartial statistics regarding health concerns and population health issues. A written informed consent was obtained from all participants before any data collection was conducted by the National Center for Health Statistics ethics review board. For this study, we utilized data from three NHANES cycles spanning from 1999 to 2004, focusing on adolescents aged 12–19 years with available information on headache, serum cotinine, and covariates. Among 7205 adolescents aged 12–19 years, 899 were excluded because their cotinine levels had not been measured. An additional 1 participant was excluded for missing data in the headache information, and a further 715 subjects were excluded due to missing values for covariates. Finally, a total of 5590 participants were included for the final analysis. The flow chart for inclusion and exclusion is shown in Fig. 1.

2.2. The definition of headache

The existence of headache was based on the self-report questionnaire “During the past 12 months, have you had frequent or severe headaches including migraine?”. The participants who reported yes to the question indicated headache sufferers.

2.3. Assessment of smoke exposure based on serum cotinine data

The nicotine metabolite cotinine in serum, measured by high-performance liquid chromatography-tandem mass spectroscopy, served as a biomarker of smoke exposure in both active smoker and non-smokers exposure to SHS. The concentrations of cotinine below the limit of detection (LOD) were substituted with LOD divided by the square root of 2. According to previous definitions, a cotinine level < 0.05 ng/mL was considered unexposed, while > 10 ng/mL was indicative of active smoking^{[17, 18]}. Furthermore, we used a threshold value of 0.316 ng/mL (the median) to define the level of exposure to SHS. Cotinine concentrations ranging from 0.05 to 0.315 ng/mL were classified as low SHS exposure, while concentrations from 0.316 to 10 ng/mL were classified as high SHS exposure.

2.4. Covariates

Our study controlled for several demographic covariates, including age, sex, race (Mexican American, non-Hispanic White, non-Hispanic Black, and Others) and poverty-income ratio (PIR). Age was dichotomized as 12–15 years old and 16–19 years old. The family poverty ratio was classified as < 1.3, 1.3–3.5, or > 3.5. In addition, the waist-to-height ratio (WHtR) was calculated and central obesity was defined as WHtR at least 0.5. Physical activity was determined by the question "Compared with most (boys/girls) your age, would you say that you are more active, less active, or about the same?”

2.5 Statistical analysis

Weighted analyses were conducted based on the complex sampling survey in accordance with the NHANES recommendations. Continuous variables were reported as the weighted means (standard deviations) or medians (interquartile ranges) and compared by adopting Student’s t test (normal distribution) or the Mann − Whitney U test (nonnormal distribution). Categorical variables were expressed as absolute values and weighted percentage and compared by a chi-square test. The serum cotinine levels were Ln-transformed for analysis because the distributions of values were highly skewed. Multivariate logistic regressions were performed to evaluate the associations to examine the association between serum cotinine and smoke exposure and headache, with 95% confidence interval and odds ratio calculated. Three models were built: Model 1, unadjusted; Model 2, adjusted for age and gender; Model 3, adjusted for all covariates. The restricted cubic splines were performed to explore the nonlinear association. To investigate the relationship between smoke exposure and headache in different subgroups, we carried out subgroup analysis, stratifying by age (12–15 years old and 16–19 years old), gender (male and female), and Central obesity (with and without). All the analyses were performed with R software, version 4.2 and p < 0.05 was regarded as statistically significant.

3.1 Baseline Characteristics

A total of 5590 adolescents aged 12 to 19 years participated in this study, with 51.60% being male and an average age of 15.47 ± 2.29 years. The median serum cotinine level was 0.14 ng/ml, and the overall prevalence of headaches was 24.99%. Smoke exposure, measured as serum cotinine levels, revealed that 751 (16.58%) participants were active smokers, 1409 (24.96%) had high SHS exposure, 1406 (22.53%) had low SHS exposure, and 2024 (35.93%) had cotinine levels < 0.05 ng/ml. Weighted baseline characteristics of smoke exposure status based on serum cotinine levels can be found in Table 1.

Table 1

Weighted baseline characteristics of smoke exposure status based on serum cotinine levels
Variable	Overall	Unexposed	Low SHS exposure	High SHS exposure	Active smoker	P-value
		Serum cotinine < 0.05 ng/ml	Serum cotinine 0.05–0.315 ng/ml	Serum cotinine 0.316 -10 ng/ml	Serum cotinine > 10 ng/ml
N (Unweighted)	5590	2024	1406	1409	751
Age, years	15.47 (2.29)	15.01 (2.17)	15.26 (2.31)	15.19 (2.30)	17.21 (1.62)	< 0.001
Gender, n(%)						0.004
Male	2814 (51.60)	942 (49.05)	692 (49.24)	703 (52.23)	477 (59.39)
Female	2776 (48.40)	1082 (50.95)	714 (50.76)	706 (47.77)	274 (40.61)
Race/ethnicity, n(%)						< 0.001
Mexican American	1970 (10.94)	1022 (15.07)	479 (12.06)	311 (7.39)	158 (5.80)
Non-Hispanic White	1463 (61.53)	550 (64.56)	279 (52.24)	352 (59.93)	282 (70.02)
Non-Hispanic Black	1697 (13.98)	298 (7.03)	513 (18.82)	643 (21.17)	243 (11.67)
Others	460 (13.54)	154 (13.34)	135 (16.88)	103 (11.52)	68 (12.50)
Family PIR, n(%)						< 0.001
< 1.3	2459 (33.53)	727 (22.32)	626 (35.38)	708 (39.80)	398 (45.89)
1.3–3.5	1978 (34.59)	735 (34.36)	499 (32.82)	514 (39.93)	230(29.43)
> 3.5	1153 (31.88)	562 (43.31)	281 (31.80)	187 (20.27)	123 (24.68)
Central obesity, n(%)
No	3480 (64.94)	1261 (69.54)	886 (63.13)	863 (60.40)	470 (64.28)	0.002
Yes	2110 (35.06)	763 (30.46)	520 (36.87)	546(39.60)	281 (35.72)
Physical activity, n(%)						0.006
Less active	852 (14.46)	307 (13.36)	205 (14.07)	210 (13.59)	130 (18.72)
Equally active	3097 (54.96)	1150 (54.26)	763 (51.41)	788 (58.83)	396 (55.43)
More active	1641 (30.58)	567 (32.38)	438 (34.52)	411 (27.58)	225 (25.85)
Serum cotinine, ng/ml	0.14 (0.02, 1.60)	0.02 (0.01, 0.04)	0.11 (0.08, 0.18)	1.05 (0.57, 2.04)	129.67 (53.15, 202.00)	< 0.001
Headache, n(%)						0.003
No	4148 (75.01)	1594 (79.32)	1032 (76.05)	1006 (71.14)	516(70.07)
Yes	1442 (24.99)	430 (20.68)	374(23.95)	403 (28.86)	235 (29.93)
Values are presented as the mean ± SD, median (interquartile range), or n (%). Abbreviations: PIR, family poverty income ratio.

We found that individuals with increasing serum cotinine levels tended to have a higher prevalence of headaches (P < 0.05). Additionally, compared to unexposed individuals (serum cotinine < 0.05ng/ml), those in the low to high SHS exposure groups were more likely to be male, non-Hispanic white, have central obesity, and come from families with poor economic status. Adolescents in the active smoking category were more likely to be older, male, non-Hispanic white, have lower family PIR, have central obesity, and engage in less physical activity compared to unexposed individuals.

3.2. Univariate analysis for headache

The univariate analysis of potential confounding factors is presented in Table 2, showing an increased risk of headaches among individuals aged 16–19 years, females, Non-Hispanic Blacks, and those with central obesity (OR > 1, P < 0.05). Conversely, adolescents from families with a PIR of 3.5 or above, and those reporting similar or reduced physical activity levels compared to their age and gender-matched peers, have a decreased risk of experiencing headaches (OR < 1, P < 0.05).

Table 2

Univariate analysis for headache in adolescents
Characteristic	OR	95% CI	P-value
Age
12–15 years	Ref
16–19 years	1.32	1.07, 1.62	0.01
Gender
Male	Ref
Female	1.54	1.22, 1.93	< 0.001
Race/ethnicity
Mexican American	Ref
Non-Hispanic White	1.03	0.85, 1.23	0.8
Non-Hispanic Black	1.41	1.17, 1.71	< 0.001
Others	1.31	0.96, 1.78	0.084
Family PIR
< 1.3	Ref
1.3–3.5	0.84	0.65, 1.07	0.2
> 3.5	0.75	0.58, 0.96	0.025
Central obesity
No	Ref
Yes	1.46	1.29, 1.66	< 0.001
Physical activity
Less active	Ref
Equally active	0.72	0.58, 0.90	0.005
More active	0.6	0.47, 0.77	< 0.001
Ref, reference; OR Odds ratio, CI Confidence interval; PIR, ratio of family income to poverty

3.3. Associations between smoke exposure and headache

Table 3 shows that log₂-transformed serum cotinine levels were consistently positively associated with the prevalence of headaches across all adjustment models (all P < 0.01). In the fully adjusted model (Model 3), a 1-unit increase in log-transformed serum cotinine was associated with a 4% higher risk of incident headaches (OR 1.04, 95% Confidence interval, CI 1.01–1.07). When serum cotinine was categorized to represent smoke exposure groups, adolescents with high SHS exposure (serum cotinine level 0.319–9.98 ng/ml) had a 39% increased risk of headaches (OR = 1.39, 95% CI 1.06–1.83, P = 0.019) compared to unexposed individuals. Additionally, adolescents who were active smokers (serum cotinine level > 10 ng/ml) also had a higher risk of headaches (OR = 1.44, 95% CI 1.01–2.05, P = 0.043). The prevalence of headaches rose with the increasing degree of smoke exposure, as determined by serum cotinine concentration (P for trend in Model 1, Model 2, and Model 3: 0.002, 0.003, and 0.011, respectively). Furthermore, the restricted cubic spline analysis revealed a positive linear association between log2-transformed serum cotinine and the prevalence of headaches in adolescents (P for nonlinearity = 0.8978; see Fig. 2).

Table 3

Weighted logistic regression analysis between serum cotinine- levels and headache risk.
	Model 1		Model 2		Model 3
	OR (95% CI)	P-value	OR (95% CI)	P-value	OR (95% CI)	P-value
Log2-Serum cotinine,	1.04 (1.02, 1.07)	0.001	1.04 (1.02, 1.07)	0.001	1.04 (1.01, 1.07)	0.008
Cotinine- verified smoke exposure categories
< 0.05 ng/ml	Ref		Ref		Ref
Low SHS exposure (0.05–0.315 ng/ml)	1.21 (0.92, 1.59)	0.2	1.20 (0.91, 1.59)	0.2	1.11 (0.83, 1.48)	0.5
High SHS exposure (0.316–10 ng/ml)	1.56 (1.18, 2.04)	0.002	1.58 (1.20, 2.08)	0.002	1.42 (1.07, 1.90)	0.018
Active smoking (> 10 ng/ml)	1.64 (1.15, 2.32)	0.007	1.64 (1.14, 2.37)	0.009	1.55 (1.06, 2.27)	0.026
p for trend	0.001		0.002		0.006
Model 1: unadjusted model. Model 2: adjusted for age and gender. Model 3: adjusted for age, gender, race, the family of poverty ratio, the waist to height ratio and physical activity. Abbreviations: Ref, reference; OR, odds ratio; CI, confidence interval; SHS, secondhand smoke.
ORs (solid lines) and 95% confidence levels (shaded areas) were adjusted for adjusted for covariates including age, gender, race, family PIR, waist-to-height ratio and self-reported physical activity

3.4 Subgroup analysis

The results of the subgroup analysis are presented in Table 4, which explores potential variations in the relationship between smoke exposure and headaches in adolescents based on age, gender, and central obesity. In the male subgroup, participants in the active smoking group and high SHS exposure group showed an 81% and 72% increased risk of developing headaches compared to unexposed participants (P < 0.05; P for trend = 0.004). In the subgroup stratified by age and central obesity, a statistically significant association was only observed in those aged 16–19 years (P for trend = 0.02) and those without central obesity (P for trend = 0.008). In addition, we performed interaction tests for gender, age, and central obesity to further commit the stability of the results in the subgroup analysis (all P for interaction > 0.05).

Table 4

Subgroup analysis for the association between smoke exposure and headache in adolescents
	smoke exposure, evaluated as serum cotinine levels, ng/ml
Characteristics	Unexposed < 0.05 ng/ml	Low SHS exposure 0.05–0.315	High SHS exposure 0.316–10	Active smoking > 10	P for trend	P for interaction
Gender						0.845
Male	Ref	1.38 (0.92, 2.08)	1.88 (1.35, 2.62)	1.81 (1.11, 2.96)	0.004
Female	Ref	0.94 (0.67, 1.31)	1.16 (0.80, 1.67)	1.45 (0.94, 2.24)	0.047
Age						0.109
12–15 years old	Ref	1.02 (0.69, 1.51)	1.29 (0.88, 1.89)	1.52 (0.81, 2.86)	0.12
16–19 years old	Ref	1.21 (0.80, 1.82)	1.6 (1.07, 2.37)	1.56 (0.98, 2.48)	0.02
Central obesity						0.881
No	Ref	1.11 (0.78, 1.57)	1.54 (1.08, 2.19)	1.61 (1.02, 2.56)	0.008
Yes	Ref	1.14 (0.74, 1.75)	1.33 (0.85, 2.07)	1.47 (0.91, 2.40)	0.098
SHS, Secondhand smoke. The results were adjusted for all covariates except the corresponding stratification variable.

This study is the first to identify the relationship between smoke exposure status and headaches in adolescents based on participants' serum cotinine levels. Our cross-sectional study, which included 5590 participants aged 12 to 19 years, revealed a significant association between smoke exposure, as assessed by serum cotinine levels, and headaches. This association was particularly pronounced in males, those aged 16–19 years, and those without central obesity. Furthermore, restricted cubic spline regression demonstrated a positive and linear association of log₂-transformed serum cotinine with the prevalence of headaches. These findings offer new epidemiological evidence linking tobacco smoke exposure, including passive or active smoking, to an increased risk of headaches in adolescents.

This study reveals a significantly higher prevalence of headaches in female subjects, older youth, individuals with central obesity, those from families of lower socioeconomic status, less active individuals, and non-Hispanic black groups, which is consistent with previous reports ^{[19, 20, 21]}. In a 1999–2004 NHANES cross-sectional study, elevated serum cotinine levels were associated with headaches in 4560 never-smoking adults^[19]. This current study focuses on adolescents as the target population. The odds of being exposed to secondhand smoke (SHS) were higher among older adolescents at home, outside the home, and in school compared with younger adolescents. Research among US adolescents found that secondhand cigarette smoke exposure in the home was a risk factor for e-cigarette susceptibility. Additionally, adolescents who smoke are more likely to become adult smokers.

Numerous cross-sectional epidemiological studies have been conducted to investigate the prevalence of headaches in adolescents and the association of adverse lifestyle factors with headaches in this population^{[20, 21]}. A cross-sectional study involving 5741 students aged 11–15 years in Croatia revealed that 23.5% students experienced headaches, which were more frequent in girls and increases with age in youth^[8]. A systematic review of population-specific studies revealed that the overall incidence of headaches in individuals under 20 years of age was 54.4%, while Abu-Arafeh estimated that 58.4% of children and adolescents experienced headaches^{[22, 23]}. Similar to results from other literature is our finding that females, have significantly higher headache than males, and the overall incidence of headache among adolescents aged 12–19 years in the United States was 25.0%, and girls accounted for 56.41%. This difference could be attributed to variations in study methods and geographic regions where the studies were carried out. Adolescent patients with headaches often experience a chronic condition characterized by near-constant or frequent attacks, leading to school absences and impacting their social relationships with family and peers. A recent meta-analysis of genome-wide association studies indicated that smoking is a risk factor for cluster headaches^[24]. Another study proposed that prolonged exposure to second-hand smoke may also contribute to its development^[25]. Our findings, along with evidence from previous studies, provide compelling grounds for implementing strategies aimed at reducing smoke exposure as a viable approach to help decrease headaches among adolescents.

Apart from epidemiological studies, the pathophysiological mechanisms underlying the association of smoke exposure with headache may be more complex^[26]. Chronic smoke exposure can increase nitric oxide levels, desensitizing cerebrovascular endothelial and smooth muscle function, which may reduce vasodilation and limit blood supply to neurons^[27]. Furthermore, SE has been shown to inhibit monoamine oxidase activity and levels in the brain. Long-term SE also causes tissue hypoxia due to chronic carbon monoxide exposure. Additionally, frequent and repeated exposure to nicotine has been proposed to sensitize pain receptors in the brain, resulting in changes in the neuromodulation of sensory information, leading to increased pain perception and reduced pain tolerance^[28].

The predominant strength of our study lies in that confirmation of such association was based on NHANES database, a nationwide investigation that involves hundreds of thousands of non-institutionalized US civilians and employs standardized study protocols, strict quality control metrics, and specialized technicians who are well-trained to collect and process data, providing a reference for comprehensively estimating the headache risk among smoke exposure adolescents across the entire country.

Our study's primary strength is its confirmation of the association based on the NHANES database, minimizing potential sources of measurement bias. This serves as a reference for a comprehensive assessment of headache risk in adolescents with tobacco exposure nationwide, highlighting the need for targeted management of tobacco exposure as a significant risk factor for adolescent headaches. However, it is important to acknowledge the study's limitations. Firstly, due to the nature of cross-sectional research, drawing causal inferences between smoke exposure and adolescent headaches is challenging. Additionally, serum cotinine, with a half-life of 18 to 20 hours, is an imperfect indicator of active or passive smoke exposure, as individuals who have quit smoking a few days before the examination may not have accurate cotinine measurements. Furthermore, the collection of headache data for adolescents in NHANES was limited to the period from 1999 through 2004, preventing validation using NHANES data from other time frames. Moreover, the observed association between smoke exposure and headaches may still be influenced by unmeasured or undermeasured covariates, potentially leading to residual confounding. Finally, our study only includes U.S. adolescents aged 12 to 19 years, so the generalizability of the findings to other populations or regions is unknown. Thus, further investigations of smoke exposure and headache in adolescents should be conducted longitudinally using larger sample sizes.

In summary, the findings indicate that smoke exposure, as indicated by serum cotinine levels, is positively associated with a higher risk of headaches in adolescents. Preventive measures and reduction of smoke exposure, including both active smoking and secondhand smoke exposure, may help protect adolescents from the risk of headaches.

NHANES	National health and nutrition examination surveys
SHS	secondhand smoke
OR	odds ratio
LOD	limit of detection
PIR	poverty-income ratio
WHtR	waist-to-height ratio
CI	Confidence interval

Acknowledgments

We thank all participants, staff, and institutions that have contributed to the NHANES database.

Authors’ Contributions

JF.W and XM.D conceptualized the research, Y.G and SS.Y collected and analyzed the data, Y.G and CL.W interpreted wrote the manuscript. JF.W and XM.D revised the manuscript. All authors contributed to the article and approved the submitted version.

Funding

This work was supported by National Natural Science Foundation of China (82302421).

Availability of data and materials

Publicly available datasets were analyzed in this study. This data can be found here: The National Health and Nutrition Examination Survey dataset at https://www.cdc.gov/nchs/nhanes/index.htm

Availability of data and materials

Publicly available datasets were analyzed in this study. This data can be found here: The National Health and Nutrition Examination Survey dataset at https://www.cdc.gov/nchs/nhanes/index.htm

Ethics approval and consent to participate

This study was reviewed and approved by NCHS Ethics Review Board. The Centers for Disease Control and Prevention (CDC) and the National Center for Health Statistics (NCHS) are responsible for conducting NHANES. All participants provided informed consent forms, and written informed consent was obtained from all the parents of the participating children who were below 16 years age.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

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No competing interests reported.

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Association between smoke exposure and headache among U.S adolescents: a cross-sectional study from the NHANES 1999-2004

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Abstract

Figures

1. Introduction

2. Materials and methods

2.1. Study population

2.2. The definition of headache

2.3. Assessment of smoke exposure based on serum cotinine data

2.4. Covariates

2.5 Statistical analysis

3. Results

3.1 Baseline Characteristics

3.2. Univariate analysis for headache

3.3. Associations between smoke exposure and headache

3.4 Subgroup analysis

4. Discussion

5. Conclusions

Abbreviations

Declarations

References

Additional Declarations

Status:

Version 1