Urinary cotinine cut-offs for tobacco smoke exposure in pregnancy and associations with child intelligence quotient: A multi-cohort analysis.

Tobacco smoke exposure not only increases the risks of lung cancer and cardiovascular disease, but can be a stressor contributing to mental illness. It is important to clarify the relationship between chronic tobacco smoke exposure and mental stress from the perspective of disease prevention. We developed a simple and highly sensitive method for simultaneously analyzing nine biomarkers: nicotine and cotinine (tobacco smoke exposure markers); cortisol, testosterone, and dehydroepiandrosterone (stress-related markers); and serotonin, melatonin, dopamine, and oxytocin (relaxation-related markers). Biomarkers were extracted and concentrated by in-tube solid-phase microextraction with a Supel-Q PLOT capillary, followed by separation and detection within 7 min using liquid chromatography–tandem mass spectrometry on a Discovery HS F5 column. Calibration curves using stable isotope-labeled internal standards showed good linearity (0.005–100 ng mL−1) with detection limits of 0.09–13.5 pg mL−1. Intra-day and inter-day precision had relative standard deviations below 7.2% and 15.5% (n = 6), respectively, with recovery rates of 84.0–108.8%. The automated method requires only ultrafiltration of hair methanol extract, enabling non-invasive pg-level analysis using just a few milligrams of hair. Hair analysis reflects an association between chronic tobacco smoke exposure and stress. This method is effective for analyzing the relationship between long-term tobacco smoke exposure and chronic stress.

Background: Tobacco smoke exposure in the home remains common among U.S. families and has been increasingly associated with adverse mental health outcomes, including anxiety and depression, among children and adolescents. Rising rates of youth anxiety and depression, coupled with evidence that secondhand smoke and related psychosocial stressors may disrupt emotional development, underscore the importance of examining household smoking exposures as a modifiable risk factor for youth mental health. This study examines associations between exposure to smoke in households and the likelihood of caregiver-reported anxiety and depression in US children and adolescents aged 6–17 years, using data from the 2022–2023 National Survey of Children’s Health (NSCH). Methods: A retrospective analysis of NSCH data for two age cohorts, children (6–11 years) and adolescents (12–17 years), for the years 2022–2023 was conducted. Descriptive statistics were generated for the selected sample by frequencies and counts for each of the dependent and independent variables, followed by binary logistic regressions for each measured mental health variable based on current diagnosis, severity levels (not severe, mild, moderate, severe) and household tobacco use. Results: This study found significant associations between parental smoking and increased odds of caregiver-reported anxiety and depression in both children and adolescents. Specifically, children living with parents who smoke had 1.55 times the odds of severe anxiety, while adolescents had 1.38 times the odds of currently experiencing anxiety and 1.31 times the odds of currently experiencing depression. Smoking inside the household was not significantly associated with caregiver-reported anxiety or depression. These findings suggest that parental smoking serves as a marker for broader psychosocial and environmental stressors that contribute to youth mental health outcomes. Conclusions: Parental smoking is a significant, modifiable risk factor for anxiety and depression among US children and adolescents. These results emphasize the need for targeted, evidence-based interventions to reduce parental smoking, improve awareness of associated mental health risks, and address social determinants of health. Policies promoting smoke-free households, integrated cessation support, and culturally tailored education programs are essential to mitigate the impact of parental smoking on child and adolescent mental health.

Passive and active tobacco smoke exposure can worsen asthma outcomes in children, yet data on its prevalence in Algeria are limited. To assess the prevalence and characteristics of tobacco smoke exposure, including prenatal and adolescent active smoking, among asthmatic children in Algeria. A multicenter cross-sectional study was conducted from December 1, 2024, to January 31, 2025, in five pediatric consultation centers across Algeria. A total of 135 children with physician-diagnosed asthma, aged 2 months to 15 years, were enrolled. Data on demographic, clinical, socioeconomic, and environmental factors were collected. Tobacco smoke exposure was documented in 37.8% of participants, most commonly attributable to paternal smoking. In utero exposure was reported in 40% of the study population. Low-income households showed a higher prevalence of exposure compared with higher-income groups (P = 0.009). The geographic distribution of exposure varied significantly (P = 0.001). No significant association was found between tobacco smoke exposure and asthma severity or asthma control. Three adolescent patients reported active smoking. Over one-third of Algerian children with asthma are exposed to tobacco smoke, with a substantial proportion exposed prenatally. These findings highlight the need for family-focused cessation programs and region-specific preventive actions to reduce children's exposure to tobacco smoke in Algeria.

Accurate sources on environmental nicotine exposure, such as biomarker data, remain insufficient in low- and middle-income countries. This study aimed to i) determine the optimal cut-off point of urinary cotinine that discriminates smokers from non-smokers, ii) estimate misclassification rate between self-reported smoking and urinary cotinine, and III) explore the distribution of tobacco smoke exposure levels using urinary cotinine concentrations among adults in Vietnam in 2024. A cross-sectional study was conducted in 2024 across seven provinces representing Vietnam's ecological regions. Using multi-level stratified random sampling techniques, 1,077 adults aged 18-60 were recruited. Demographic and behavioural data were obtained through structured interviews. Urinary cotinine to creatinine ratios (CCR) were measured using high-performance liquid chromatography-tandem mass spectrometry. The Youden J method was used to determine the optimal cut-off point of CCR. Statistical analyses were performed using SPSS 20.0. Self-reported results showed that 18.3% were active smokers, 33.4% were exposed to SHS at home, and 48.3% lived in a non-smoking household. The optimal CCR cut-off value of 20.947 µg/g can distinguish smokers and non-smokers with a sensitivity of 61.5%, specificity of 93.2%, 70.6% positive predictive value and 90% negative predictive value. Regional disparities and urinary cotinine among the non-smoking groups suggest potential environmental exposure to nicotine. The CCR level of 20.947 µg/g indicated the optimal cut-off value to distinguish smokers and non-smokers. Vietnam was among countries with high levels of environmental nicotine exposure, with significant variation by sex, education, occupation, income, and region. Urinary cotinine is a reliable biomarker for nicotine exposure and should be integrated into routine surveillance. These findings support the need for stricter enforcement of smoke-free environments and interventions tailored to reduce involuntary tobacco exposure.

Background: Prostate cancer in the Middle East and North Africa (MENA) region is shaped by a complex interplay of behavioral and environmental risk factors, yet comprehensive estimates of preventable cases remain scarce. To address this gap, we estimated population-attributable fractions (PAFs) for a range of modifiable exposures among men aged 50 years and older and assessed potential reductions in incidence under feasible intervention scenarios. Methods: Regional prevalence data were combined with relative risks from meta-analyses to compute closed-form PAFs for tobacco smoking, obesity, physical inactivity, high dairy and calcium intake, heavy alcohol use, drinking water nitrates, trihalomethanes, arsenic, lead, selenium status, ambient PM2.5 and NO2, and occupational diesel exhaust, covering an estimated 47 million men. Estimates were validated using a synthetic cohort simulation of 100,000 individuals, with uncertainty quantified through Monte Carlo sampling. Results: Results showed that drinking water nitrate exposure accounted for the largest single fraction (17.4%), followed by tobacco smoking (9.5%), physical inactivity (6.7%), and trihalomethane exposure (5.0%), while other exposures contributed smaller but meaningful shares. Joint elimination of all exposures projected a 45.5% reduction in incidence, and simultaneous feasible reductions in four targeted exposures yielded a combined potential impact fraction of 12.1%. Conclusions: These findings suggest that integrated water quality management, tobacco control, lifestyle interventions, and targeted environmental surveillance should be prioritized to reduce prostate cancer burden in the MENA region. However, estimates of drinking-water nitrate exposure rely on limited evidence from a single case–control study with a relatively small sample size, and should therefore be considered exploratory and primarily hypothesis-generating.

Autism spectrum disorder (autism) describes a heterogeneous neurodevelopmental phenotype arising from the interplay of environmental and genetic factors in early life. In a general population birth cohort, we employed a scoping approach to identify prospective associations between prenatal and birth factors and a subsequent autism diagnosis. Factors associated with increased likelihood of autism included those related to i) maternal health (maternal pre-pregnancy body mass index, pre-existing maternal mental health conditions, maternal use of selective serotonin reuptake inhibitors) ii) environmental exposures (maternal passive tobacco smoke exposure, and exposure to vinyl floors) iii) demographic factors (socioeconomic disadvantage). Factors associated with a decreased likelihood of autism included maternal dietary nutrition and supplementation (higher folic acid, magnesium, and iron, as well as adherence to the Australian Dietary Guidelines). Our findings extend the evidence that autism may have a multifactorial origin in early life. Further studies should explore the composite effects of these prenatal and birth factors on autism outcomes via shared biological pathways, such as inflammation, and oxidative stress, in concert with genetic predisposition. Autism spectrum disorder (autism) is a multifactorial condition. Here we report on multiple prenatal environmental, demographic, maternal and pregnancy factors that are associated with an increased likelihood of an autism diagnosis. For example, adherence to the Australian Dietary Guidelines during pregnancy is linked to a reduced likelihood of autism in the offspring, consistent with mounting evidence that prenatal nutrition impacts brain development. We examine how the multiple risk factors, identified by our comprehensive approach, may be linked to shared biological mechanisms. Future work should examine composite exposure measures acting through shared mechanisms as a more productive approach to understanding aetiology than focusing solely on individual exposures.

Background: Chronic obstructive pulmonary disease (COPD) remains a major cause of morbidity and mortality worldwide, with limited therapeutic efficacy in current treatment regimens. Non-pharmacological approaches such as phototherapy and magnetotherapy may offer adjunctive benefits. Objective: To evaluate the clinical efficacy, immune response modulation, and bronchial patency improvement associated with pulsed visible-spectrum phototherapy combined with magnetotherapy in COPD patients at early rehabilitation stages, and to assess the corresponding effects on macrophage function in an experimental COPD rat model. Methods: Sixty-three patients with COPD stages I–II were enrolled and divided into main (n = 28) and control (n = 35) groups. The main group received pulsed phototherapy using a “SLU-2” device on lung root projections in addition to standard magnetotherapy, while the control group received magnetotherapy alone. Both groups underwent functional, immunological, and cytological evaluations pre- and post-treatment. An experimental COPD model in rats was induced via chronic tobacco smoke exposure, followed by similar phototherapy protocols for macrophage assessment. Results: Post-treatment, the main group exhibited significant reductions in cough severity, dyspnea, and obstructive symptoms (p < 0.05). Forced expiratory volume in one second (FEV₁) and forced vital capacity (FVC) increased by 1.5-fold and 1.2-fold, respectively. Mid-expiratory flows improved significantly. Immunological assays showed enhanced T-lymphocyte proliferation and helper cell counts. Cytological analysis revealed increased phagocytic leukocyte activity and progression to epithelialization stages. In the rat model, macrophage enzymatic activity significantly increased following phototherapy (p < 0.05). Conclusions: Combined pulsed phototherapy and magnetotherapy significantly improved pulmonary function, enhanced immune responses, and promoted nonspecific cellular defense in COPD patients without adverse cardiovascular effects. These findings support the integration of phototherapy modalities into COPD rehabilitation protocols.

Arsenic is a pervasive environmental contaminant and a recognized global public health concern. Experimental evidence suggests that arsenic may disrupt endocrine signaling during critical developmental windows, yet epidemiologic data on its effects on thyroid function in early childhood remain limited. We investigated the cross-sectional association between arsenic exposure and free thyroxine (fT4) levels among 496 children aged 5 to 7 years enrolled in the Bangladesh Environmental Research in Children's Health (BiRCH) cohort. Arsenic exposure was assessed using urinary total arsenic and toenail arsenic concentrations. Serum fT4 levels were measured by an enzyme-linked immunosorbent assay (ELISA) kit. Associations with fT4 were estimated using multivariable linear regression models adjusted for child age, sex, body mass index, and environmental tobacco smoke exposure. The median urinary and toenail arsenic concentrations were 88.0µg/L (interquartile range [IQR]: 127.4) and 1.7µg/g (IQR: 2.0), respectively. Children in the highest quartile (Q4) of arsenic exposure had significantly higher fT4 levels compared to those in the lowest quartile (Q1), for both urinary (β = 0.09; 95% CI: 0.005-0.17) and toenail arsenic (β = 0.10; 95% CI: 0.03-0.17). A significant dose-response trend was observed across quartiles, suggesting a potential linear relationship. Our findings suggest that thyroid function may be a sensitive target of arsenic toxicity in early childhood. Longitudinal studies are necessary to assess the long-term effects of early-life arsenic exposure on thyroid function across the life course.

Chronic obstructive pulmonary disease (COPD) is a heterogeneous, progressive pulmonary disorder with persistent respiratory symptoms resulting from abnormalities in the airways and/or alveoli and was prevalent globally in 10.3% of people aged 30-79 years in 2019. The prevalence of COPD has increased rapidly in women in the past decade. This may be due to increased tobacco use, but may also involve sex-specific factors. To evaluate the prevalence of COPD in the context of sex and tobacco exposure. Comprehensive searches of MEDLINE (OVID), EMBASE and CENTRAL were conducted for articles published from inception to July 22, 2022. We independently evaluated titles, abstracts and full-text articles in a duplicated two-staged process. Studies were included if they reported the prevalence of COPD as a primary outcome in the context of sex and tobacco exposure. Pooled analysis was conducted with Review Manager 5, and heterogeneity was assessed with the I2 statistic. For 163, 450 individuals the prevalence of COPD was 3.5-20.7% in males and 6.3-18.5% in females, and we observed a non-statistically significant difference of 1.53% [95% CI: -5.83, 8.89] (p = 0.68) in females compared to males with tobacco exposure (Tau2 = 54.02; Chi2 = 53.15; df = 4 (P < 0.00001); I2 = 92%). Females with COPD had earlier mortality, greater co-morbidities involving cardiovascular disease and others, and decreased FEV1% predicted, as compared to males with COPD. Estrogen and androgens may protect against COPD, but smoking-induced hypogonadism may diminish these effects. Menopause could also be a contributor to worse COPD outcomes. Included articles are limited by the quality of data on tobacco smoke exposure, primarily reported as a binary risk factor, with lack of availability on duration and intensity of exposure. There was earlier mortality and reduced FEV1 in females with COPD, as compared to males with COPD. Thus, sex-specific considerations are important in understanding the pathophysiology of COPD and should be a focus of further research.

Association of early-life tobacco smoke exposure with chronic gastrointestinal diseases in adulthood and trajectory of chronic gastrointestinal multi-morbidity: A large prospective cohort study.

Prenatal smoke exposure impairs fetal lung development, but the interplay between cotinine, oxidative stress, and early respiratory dysfunction remains unclear. This study aimed to quantify the effects of prenatal smoke exposure on neonatal respiratory function and develop a validated predictive model to identify this dysfunction. This prospective cohort study included term newborns with prenatal tobacco smoke exposure (n = 50) and healthy controls (n = 41). Cord blood cotinine, oxidative stress markers, and tidal breathing parameters assessed at 48 h post-delivery were compared. A decision tree model was developed and rigorously validated for performance, calibration, and temporal stability to predict decreased expiratory flow. Smoke-exposed newborns exhibited significantly impaired expiratory flow (p < .001), elevated cord cotinine (p < .001), and increased systemic oxidative stress (p < .05). The decision tree model selected a cord blood cotinine level >26.1 ng/mL as the primary predictor, conferring a 94% probability of dysfunction. For those with lower cotinine, a total oxidant status >9.75 μmol/L was a secondary predictor (87.5% probability). The final model achieved 72.5% accuracy and demonstrated good calibration. Prenatal smoke exposure induces quantifiable neonatal respiratory dysfunction mediated by oxidative stress. Cord blood cotinine and total oxidant status are robust biomarkers for risk stratification. Our validated decision tree offers a practical framework for identifying respiratory dysfunction in newborns.

To determine the prevalence, risk factors for perinatal tobacco smoking, and the effects on infants' respiratory health in 12,450 mother-infant pairs from South America. Cross-sectional population-based study in eleven centres from six countries, using a standardised questionnaire completed by parents. The prevalence of smoking during pregnancy was 8.4%, ranging from 1.4% in Lima to 15.3% in Montevideo; current maternal smoking was 15.3%, from 5.4% in Lima to 34.4% in Santiago; and second-hand tobacco smoke (SHS) at home was 29.8%, from 13.7% in Lima to 50.7% in Santiago. SHS and current maternal smoking were strong and independent risk factors for smoking during pregnancy (p < 0.0001). Low maternal education and monthly household income were significant risk factors for perinatal tobacco exposure. The prevalence and severity of wheezing, admissions for wheezing, pneumonia diagnosis, and admissions for pneumonia were significantly higher (p < 0.0001) in infants exposed to tobacco smoke. The prevalence of smoking during pregnancy, current maternal tobacco smoking, and SHS remain high in South America. Perinatal tobacco smoke exposure is strongly related to greater wheezing severity and a higher prevalence of admissions for wheezing and pneumonia during the first year of life. Low socioeconomic status and low maternal education were the most significant risk factors for smoking during pregnancy, as well as for current maternal smoking and the presence of SHS at home. Our results point to the urgent need to improve the quantity and quality of education against tobacco smoking in girls and families, starting very early in life.

A non-smoker who is exposed to second-hand tobacco smoke is in danger of suffering from diseases such as coronary heart disease, asthma attacks, stroke and lung cancer. This exposure occurs in various set tings, including living with smokers at home, visiting bars and casinos, public places, and transport vehicles. Additionally, individuals exposed to second-hand tobacco smoke may experience severe health risks includ ing deaths. To gain insights about the dynamics of second-hand tobacco smoke exposure and its associated health risks to non-smokers, a deterministic mathematical model is developed and analysed. Such a model is developed by using non-linear first order ordinary differential equations and the analysis was carried out ana lytically and numerically. Numerical simulation results in this study confirm that, 90% increase in interaction between smokers and non-smokers can increase health risks to non-smokers by 7%. Additionally, the formu lated system exhibits backward bifurcation implying the possibility of having large outbreaks of health risks related to second-hand tobacco smoke even in communities with a relatively small number of smokers. The study underscores the importance of interventions to mitigate the health risks associated with second-hand tobacco smoke. Specifically, efforts should focus on reducing interactions between smokers and non-smokers during smoking or providing robust support mechanisms to help smokers quit.

Background: Tobacco smoke exposure is the leading cause of chronic obstructive pulmonary disease (COPD). In India, bidi smoking is common, yet its effects on vascular health and lung function are underreported. This study compares pulmonary function and carotid intima-media thickness (CIMT) between bidi and cigarette smokers with COPD. Methods: Thirty-one stable COPD patients were classified based on primary tobacco exposure: bidi (n = 17) or cigarette (n = 14) smokers. Spirometry was performed to assess FEV1, and CIMT was measured using high resolution B-mode ultrasonography. Smoking history, symptom severity, and cardiovascular parameters were recorded and compared. Results: Bidi smokers had lower mean FEV1 (38.3%) than cigarette smokers (45.2%) and higher mean CIMT values (1.56 mm vs. 1.26 mm). Despite fewer pack-years in some bidi smokers as compared with cigarette smoking, vascular and pulmonary damage was more pronounced. Bidi users had more advanced GOLD staging and higher dyspnea scores. Conclusion: Bidi smoking is associated with greater impairment in both pulmonary and vascular function than cigarette smoking in COPD patients. These findings suggest that bidi smoke may exert disproportionately toxic effects and that public health policies should address this overlooked risk.

Atopic eczema and asthma frequently co-occur, forming a distinct complex phenotype that likely arises from shared genetic pathways and early-life environmental influences. We aimed to investigate whether variants in TNS1 and NRXN1—previously identified in a genome-wide interaction study—influence susceptibility to atopic eczema and the asthma–eczema phenotype and whether early-life environmental tobacco smoke (ETS) exposure modifies these genetic effects. A total of 188 Caucasian children under 2 years at recruitment were prospectively followed up to 6 years of age. Eligibility of all participants for the study or control group was based on a questionnaire and a physician-confirmed diagnosis of eczema and asthma. Early-life ETS exposure was assessed by parental questionnaire. All participants were genotyped for TNS1 and NRXN1 SNPs. The TNS1 rs918949 [T] allele was associated with the combined asthma–eczema phenotype but not with eczema alone. Synergistic gene–environment interactions were identified for both TNS1 and NRXN1, with the highest risk of the combined asthma–eczema phenotype observed among ETS-exposed carriers of risk alleles. Our findings provide the first independent replication of evidence suggesting that TNS1 and NRXN1 may contribute to the asthma–eczema comorbidity through mechanisms that could be substantially modified by early-life ETS exposure.

The aim of this study was to examine associations involving serum proprotein convertase subtilisin/kexin type 9 (PCSK9) in metabolic disturbances observed in women with polycystic ovary syndrome (PCOS), with particular emphasis on the potential impact of tobacco smoke exposure. The study included 88 women: 60 with PCOS (23 smokers and 37 non-smokers) and 28 without PCOS. Selected biochemical and molecular biomarkers related to lipid metabolism, oxidative stress, and inflammation were assessed. No significant differences in PCSK9 levels were observed among non-smoking women with PCOS, smoking women with PCOS, and non-smoking women without PCOS. However, in women with PCOS, excess body weight and insulin resistance were associated with increased PCSK9 concentrations. Significant correlations between PCSK9, lipid profile parameters, and the Castelli and triglycerides-glucose indices suggest a potential role of PCSK9 as a biomarker of dyslipidemia and cardiometabolic risk. Elevated PCSK9 levels may contribute not only to increased low-density lipoprotein cholesterol but also to enhanced formation of oxidized low-density lipoprotein, which is particularly detrimental to cardiovascular and metabolic health. Vitamin D levels were more strongly associated with smoking status and insulin resistance than with excess body weight. Overall, these findings indicate that PCSK9 regulation in PCOS may be driven predominantly by metabolic factors rather than PCOS status or smoking per se, and that metabolic status and vitamin D deficiency should be considered when assessing cardiometabolic risk in this population.

Lung cancer remains one of the leading causes of cancer-related mortality worldwide and is strongly associated with tobacco smoke exposure. In recent years, electronic cigarettes have gained popularity as seemingly safer alternatives to conventional cigarettes; however, their impact on tumor biology remains controversial. A central process in lung cancer progression is the epithelial–mesenchymal transition (EMT), which promotes cellular invasion, migration, and therapy resistance. This review summarizes current evidence on how nicotine, polycyclic aromatic hydrocarbons (PAHs), carbonyl compounds, and reactive oxygen species (ROS) modulate EMT through key signaling pathways, including PI3K/AKT, MAPK/ERK, Wnt/β-catenin, Notch, and HIF-1α. Moreover, it discusses the role of thermal processes during tobacco combustion and e-liquid heating in generating carcinogenic by-products. Emerging data indicate that both traditional and electronic cigarettes release bioactive agents capable of inducing EMT, thereby contributing to lung cancer pathogenesis and revealing potential therapeutic targets.

Inflammation underpins pulmonary disease progression during tobacco smoke exposure, which may culminate in irreversible pulmonary disease. While primary smoke poses a notable risk, nearly half of the US population is also susceptible due to frequent exposure to secondhand smoke (SHS). In the present study, we assessed the potential role of VYN202, a novel small molecular bromodomain and extra-terminal inhibitor, as a possible means of attenuating SHS-mediated inflammation. We exposed wild-type mice to an acute time course of room air (RA), SHS via a nose-only delivery system (Scireq Scientific, Montreal, Canada), or to both SHS and 10 mg/kg VYN202 (efficacious dose from prior inflammatory models) via oral gavage three times a week. Specific smoke exposure delivery to mice involved SHS from two cigarettes over 10 min, equilibration in room air for 10 min, followed by exposure to SHS from one cigarette for an additional 10 min, for a total SHS exposure of 20 min per day, five days a week for 30 days. We evaluated leukocyte abundance and the secretion of inflammatory mediators in bronchoalveolar lavage fluid (BALF). We also assessed general morphology via histology staining and the activation of receptor tyrosine kinase (RTK) family members. While standard hematoxylin and eosin (H&E) staining resulted in unchanged morphology, SHS-mediated increases in BALF protein abundance, total cellularity, and percent PMNs were attenuated with concomitant administration of VYN202. We also discovered SHS-induced activation of RTKs that were pro-inflammatory (JAK1, JAK3, ABL1, and ACK1), as well as RTKs related to endothelial and vascular remodeling (VEGFR3, VEGFR2, EphB4, EphB6, and FAK). Furthermore, inflammatory cytokines including GCSF, IFN-γ, IL-12p70, IL-17A, LIX, and TNF-α were all augmented by SHS exposure. Despite SHS exposure, each of these RTKs and cytokines/chemokines was significantly attenuated by VYN202. In summary, inflammatory responses induced by SHS exposure were mitigated by VYN202. These data reveal fascinating potential for the utility of VYN202 in lessening smoke-induced pulmonary exacerbations.

Hypertension is a major modifiable risk factor for cardiovascular disease in South Asia, especially in Pakistan. In the meantime, ambient air pollution in Peshawar and other urban areas is quite high, particularly fine particulate matter (PM₂.¹), which is increasingly associated with elevated blood pressure through inflammatory and vascular processes. Nevertheless, Peshawar currently lacks local data linking long-term exposure to PM₂.¹ to hypertension. Objectives: To find out how common hypertension is among urban Peshawar inhabitants, evaluate long-term exposure to ambient PM₂.¹, and investigate the relationship between PM₂.¹ exposure and hypertension. Methods: 384 people who were at least eighteen years old and had been in metropolitan Peshawar for at least five years took part in a cross-sectional survey over the course of five months. The participants were chosen using a multistage random selection technique. Data was gathered using a systematic questionnaire that was adapted from widely used worldwide instruments, including the WHO Household Energy and Air Pollution Survey, the American Thoracic Society questionnaire, and WHO STEPS. We gathered information on tobacco smoke exposure, PM₂.¹ exposure markers, respiratory symptoms, hypertension, and sociodemographic characteristics. The data was analyzed using SPSS version 26. Relationships were assessed using chi-square tests, and descriptive statistics were calculated with statistical significance set at p &lt; 0.05. Results: In 31.8% of cases, hypertension was diagnosed. Approximately 27.6% of the participants lived near major pollution sources, and 84.1% reported spending at least two hours outside every day. Half of the participants reported having a family history of hypertension. Of those surveyed, 23.4% admitted to smoking tobacco, and 49.2% said they had been in close contact to secondhand smoke. Respiratory problems were common, with 28.4% reporting dyspnea and 27.6% reporting a chronic cough. The findings demonstrate the substantial impact of hypertension on a population exposed to high ambient PM2 levels. Conclusion: In metropolitan Peshawar, where prolonged exposure to high PM2.0 air pollution levels is common, hypertension is significantly more common in adults. These results highlight the critical need for coordinated environmental and public health initiatives to lower pollution and enhance hypertension prevention and treatment in Pakistani cities. They also corroborate the evidence that ambient air pollution raises blood pressure.