Patil Sneha S, Puttaswamy Naveen, Pillarisetti Ajay, Cardenas Andres, Steenland Kyle, Patil Smita S, Saidam Sudhakarao, Bharadwaj Rangarajan, Balakrishnan Kalpana, Waller Lance A, Peel Jennifer, Clasen Thomas, Barr Dana Boyd
Department of Environmental Health Engineering, Faculty of Public Health, Sri Ramachandra Institute of Higher Education and Research, Chennai, Tamil Nadu, India; Department of Pediatric and Preventive Dentistry, Dr. D.Y. Patil Dental College and Hospital, Dr. D.Y. Patil Vidyapeeth, Sant-Tukaram Nagar, Pimpri, Pune, India.
Department of Environmental Health Engineering, Faculty of Public Health, Sri Ramachandra Institute of Higher Education and Research, Chennai, Tamil Nadu, India.
Environ Res. 2025 Oct 1;282:122021. doi: 10.1016/j.envres.2025.122021. Epub 2025 May 30.
Exposure to polycyclic aromatic hydrocarbons (PAH), generated through incomplete combustion of organic materials such as coal and wood, and through activities, like charbroiling meat and smoking tobacco, negatively impact children's health. This study evaluates early-life PAH exposure in children from Southern India and its association with early childhood caries (ECC).
We utilized maternal and child urine samples from the Household Air Pollution Intervention Network (HAPIN) cohort to measure PAH metabolites: 2-naphthol (2-NAP) and 1-hydroxypyrene (1-PYR). We evaluated presence of dental caries in children (n = 712) using decayed, missing, and filled surfaces (dmfs) index. Socio-demographic data and dietary recall information were collected through questionnaires. Data analysis was conducted using a negative binomial hurdle model.
Dental caries prevalence was high, with 53.6 % of participants having cavitated lesions, 13.6 % showing non-cavitated lesions, and 32.8 % classified as caries-free. Elevated urinary concentrations of 2-NAP during first and third trimesters were associated with a 1.09-fold increase in caries incidence (95 % CI, 1.03-1.16 and 1.02-1.17, respectively). Postnatal exposure to 1-PYR at six months corresponded to an 8 % increase in ECC risk per log-unit rise (IRR, 1.08; 95 % CI, 1.02-1.16). Average postnatal PAH exposure (mean 96.55 μg/g creatinine) demonstrated a stronger link with each log-unit increase corresponding to an incident rate ratio (IRR) of 1.22 (95 % CI, 1.10-1.36) in the count model and an odds ratio (OR) of 1.36 (95 % CI, 1.06-1.63) in zero model. Categorical analyses revealed monotonic dose-response relationships, with children in the highest quartile of postnatal 2-NAP and 1-PYR exposure exhibiting 39 % and 35 % greater ECC burden, respectively, compared to those in the lowest quartile.
Our findings suggest an association between PAH exposure and ECC, particularly during the first and third trimesters with lifestyle factors playing a modifying role. The compounded impact of co-exposure to smoke from secondhand smoke and biomass-based cooking underscores critical need to reduce PAH exposure during early childhood.
接触多环芳烃(PAH)会对儿童健康产生负面影响,PAH可通过煤和木材等有机材料不完全燃烧以及烤肉和吸烟等活动产生。本研究评估了印度南部儿童早年接触PAH的情况及其与幼儿龋齿(ECC)的关联。
我们利用家庭空气污染干预网络(HAPIN)队列中的母婴尿液样本测量PAH代谢物:2-萘酚(2-NAP)和1-羟基芘(1-PYR)。我们使用龋齿、缺失和填充牙面(dmfs)指数评估了儿童(n = 712)的龋齿情况。通过问卷调查收集社会人口统计学数据和饮食回忆信息。使用负二项式障碍模型进行数据分析。
龋齿患病率很高,53.6%的参与者有龋洞病变,13.6%有非龋洞病变,32.8%无龋齿。孕早期和孕晚期尿中2-NAP浓度升高分别与龋齿发病率增加1.09倍相关(95%CI,分别为1.03 - 1.16和1.02 - 1.17)。出生后6个月接触1-PYR,每log单位增加对应ECC风险增加8%(IRR,1.08;95%CI,1.02 - 1.16)。出生后PAH平均暴露量(平均96.55μg/g肌酐)在计数模型中显示与每log单位增加有更强的关联,对应发病率比(IRR)为1.22(95%CI,1.10 - 1.36),在零模型中优势比(OR)为1.36(95%CI,1.06 - 1.63)。分类分析显示出单调剂量反应关系,出生后2-NAP和1-PYR暴露最高四分位数的儿童与最低四分位数的儿童相比,ECC负担分别高出39%和35%。
我们的研究结果表明PAH暴露与ECC之间存在关联,特别是在孕早期和孕晚期,生活方式因素起调节作用。二手烟和生物质烹饪烟雾共同暴露的复合影响凸显了在幼儿期减少PAH暴露的迫切需求。