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Introduction: Tobacco use and exposure to Second-Hand Smoke (SHS) are major health hazards for growing children and adolescents. Smokeless Tobacco (SLT) product consumption is a serious health issue both abroad and in India. Children and young people are more likely to be exposed to Secondhand Smoke (SHS) in India due to high population density. Aim: To assess physical anthropometric parameters and cardiac autonomic function tests among passive smokers and SLT users. Materials and Methods: This cross-sectional study was conducted in the department of Physiology Nootan Medical College and Research Centre, Visnagar from August 2023 to February 2024. The study was comprised of 100 participants including 50 non-smokers who chew tobacco and who have never been a passive smoker in Group-A (SLT) and 50 age-matched passive smokers who lived with at least one smoker or frequently interacted with smokers at work for at least three years before conducting this study was included in Group-B (Passive smoke or SHS). Anthropometric measurements were recorded. Cardiac autonomic function tests were done by using a Polyrite recording machine with mode “ECG” in Lead-II position among both groups. Results were expressed as mean±Standard Deviation (SD), and analysed by using unpaired student’s t-test. The p-value of

Introduction: Tobacco use and exposure to Second-Hand Smoke (SHS) are major health hazards for growing children and adolescents. Smokeless Tobacco (SLT) product consumption is a serious health issue both abroad and in India. Children and young people are more likely to be exposed to Secondhand Smoke (SHS) in India due to high population density. Aim: To assess physical anthropometric parameters and cardiac autonomic function tests among passive smokers and SLT users. Materials and Methods: This cross-sectional study was conducted in the department of Physiology Nootan Medical College and Research Centre, Visnagar from August 2023 to February 2024. The study was comprised of 100 participants including 50 non-smokers who chew tobacco and who have never been a passive smoker in Group-A (SLT) and 50 agematched passive smokers who lived with at least one smoker or frequently interacted with smokers at work for at least three years before conducting this study was included in Group-B (Passive smoke or SHS). Anthropometric measurements were recorded. Cardiac autonomic function tests were done by using a Polyrite recording machine with mode "ECG" in Lead-II position among both groups. Results were expressed as mean±Standard Deviation (SD), and analysed by using unpaired student's t-test. The p-value of <0.05 was considered as statistically significant. Results: Resting (Basal) heart rate was significantly increased in the SLT group (p-value=0.001). Resting Systolic Blood Pressure (SBP) was significantly reduced in the passive smoker group when compared to SLT group (p-value=0.001). It was noted that 30:15 ratio was statistically significant in the passive smokers as compared to that in the SLT group (p-value=0.001). It was also noted that blood pressure response to immediate standing in passive smokers was highly significant (p-value=0.001). Conclusion: The results of present study showed that sympathetic activity was increased and parasympathetic activity was decreased in tobacco users (SLT). The fall of SBP in response to immediate standing among passive smokers is suggestive of decreased central sympathetic activity and baroreceptor reflex sensitivity. [ABSTRACT FROM AUTHOR]

Abstract Background Particulate matter (PM) emission caused by tobacco combustion leads to severe health burdens worldwide. Second-hand smoke exposure is extraordinarily high in enclosed spaces (e.g., indoor rooms, car cabins) and poses a particular threat to the health of vulnerable individuals (e.g., children, elderly, etc.). This study aimed to establish a new measuring platform and investigate PM emissions under four different ventilation conditions inside a car cabin without exposing any person to harmful tobacco smoke. Methods PM concentrations were measured during the smoking of 3R4F reference cigarettes in a Mitsubishi Space Runner (interior volume 3.709 m3). The cigarettes were smoked with a machine, eliminating exposure of the researchers. Cigarettes were extinguished 4.5 min after ignition, and PM measurements continued until 10 min after ignition. Results High mean PM concentrations were measured for cigarettes without ventilation after 4.5 min (PM10: 1150 µg/m3, PM2.5: 1132 µg/m3, PM1: 861.6 µg/m3) and after 10 min (PM10: 1608 µg/m3, PM2.5: 1583 µg/m3, PM1: 1133 µg/m3). 3R4F smoked under conditions with turned on ventilation resulted in reduction of PM compared to those smoked without ventilation after 4.5 min (PM10:-47.5 to -58.4%, PM2.5:-47.2 to -58%, PM1:-39.6 to -50.2%) and after 10 min (PM10:-70.8 to -74.4%, PM2.5:-70.6 to -74.3%, PM1:-64.0 to -68.0%). Cigarettes smoked without ventilation generated high PM peaks at 4.5 min (PM10: 2207 µg/m3, PM2.5: 2166 µg/m3, PM1: 1421 µg/m3) and at 10 min (PM10: 1989 µg/m3, PM2.5: 1959 µg/m3, PM1: 1375 µg/m3). PM peaks of cigarettes smoked under different ventilation modes varied at 4.5 min (PM10: 630-845 µg/m3, PM2.5: 625-836 µg/m3, PM1: 543 - 693 µg/m3) and 10 min (PM10: 124 - 130 µg/m3, PM2.5: 124 - 129 µg/m3, PM1: 118 - 124 µg/m3). Conclusion The new measuring platform provides a safer way for researchers to investigate PM emissions of cigarettes. These data are comparable to published research and show that smoking in a parked vehicle with the windows closed generates harmful PM emissions even when the vehicle ventilation is in operation. Future studies should be carried out using the new measuring platform investigating PM exposure and PM distribution of in-vehicle smoking under a wide range of conditions.

Introduction: Second-hand smoke is formed from the burning of smoking products and the smoke exhaled by the smokers. Worldwide, a large proportion of children, male and female non-smokers are exposed to the second-hand smoke at home. Exposure to second-hand smoke resulted in the occurrence of several diseases such as ischaemic heart disease, lower respiratory infections, asthma and lung cancer, and even death. With the growing scientific evidences for the hazard of Second-hand smoke, many countries have taken stringent action to reduce Second-hand smoke exposure through legislation and health education, and have achieved significant improvements. Materials and methods: This is a prospective and cross-sectional study conducted in the Department of Community Medicine at Tertiary Care Teaching Hospital over a period of 1 year; we objectively assessed SHS exposure concentrations. A predesigned, pretested semi structured interview schedule was prepared and translated into the local language. We used two measures of SHS: exposure to SHS at home and exposure to SHS in the workplace. SHS exposure at home is estimated for non-smokers who reported anyone smoking inside his/her home. Exposure to SHS in the workplace is estimated for non-smokers who reported anyone smoking in the workplace in the past 30 days before the survey. Result: In this study shows the demographic predictors of SHS at home and workplace. At home and workplace, the SHS exposure was higher among male (89%) as compared to female (11%), whereas at home, the SHS exposure was higher among male (82.5%) as compared to female (17.5%) and at workplace, the SHS exposure was higher among male (90.9%) as compared to female (9.1%). Distribution of Age group of persons exposed to second-hand smoke at home and workplace, the exposure was highest in 25-44 years old (52.7%) while lowest years old have exposure to SHS as compared to other age group categories. Distribution of Residence of persons exposed to second-hand smoke at home and workplace at urban area (62.7%) as compared to rural settings (37.2%). The high-grade education category was (30.9%) had the highest exposure to SHS at the workplace in contrast to other categories. The Retired and unemployed occupation category (3.6%) had the highest exposure to SHS analogous to other occupation categories. Conclusion: Current smoking and exposure to second-hand smoke among internal migrants in India is high. Socio-demographic characteristics and migration status were strongly associated with current smoking and second-hand smoke exposure. We recommend specifically targeted tobacco control interventions to help to address these risk factors. [ABSTRACT FROM AUTHOR]

Introduction: Cannabis is a widely used drug like tobacco and alcohol. In the meantime, it is also prescribed for medical treatment in some countries. Tobacco smoke contains chemical carcinogens and particulate matter (PM) that are both harmful to health. Method: In this study, we investigated PM levels in second-hand smoke (SHS) of hand-tamped cannabis cigarettes compared to cigarettes with tubing tobacco and the 3R4F reference cigarette. Results: It could be demonstrated that the largest proportion of the particle mass is attributable to particles with a diameter of less than 1μm and that every tested cigarette emitted more PM than the 3R4F reference cigarette. In addition, our data clearly revealed that cannabis smoke contains higher PM levels in SHS than tobacco cigarettes. Compared to the reference cigarette, the PM 1 emissions of cannabis were 105% higher. Also, the cannabis mixed cigarettes had higher PM levels than the 3R4F cigarettes. For instance, the PM 10 emissions were 93% higher. Also, the Gauloises Mélange tubing tobacco also reached higher PM concentrations than the 3R4F cigarette. Discussion: Regardless of negative health effects, cannabis is seen as a harmless drug in the public eye. We found strong indications for potential health risks by PM from cannabis products and, therefore, the public should be educated about a potential harm.

Aim: The aim of this study was to estimate the percentage and sources of secondhand smoke (SHS) exposure among non-smoking pregnant women. It was a cross-sectional study conducted among the non-smoking pregnant women registered at the primary health center (PHC) under the All India Institute of Medical Science (AIIMS), Rishikesh. Materials and Methods: All registered pregnant women at sub-center in the field practice area (Raiwala) of the Department of Community and Family Medicine, AIIMS Rishikesh were recruited in the study. In this study, a questionnaire was used for measuring the exposure of SHS. Mean and standard deviation (SD), median, minimum, and maximum were used for continuous variables. A Chi-square test was used to compare the association of categorical variables. Results: Out of the total participants, 62% were exposed to SHS. 33% of participants were exposed to SHS at home only, 24% at public places only, and 5% were the ones exposed both at home and public places. More than half (69%) of the participants were having inadequate knowledge about the harms caused by SHS. Conclusions: More than half of the participants were exposed to SHS. Inadequate knowledge among the participants about adverse effects of SHS exposure and insufficient practices and action were observed.

Background: Particulate matter (PM) emission caused by tobacco combustion leads to severe health burdens worldwide. Second-hand smoke exposure is extraordinarily high in enclosed spaces (e.g., indoor rooms, car cabins) and poses a particular threat to the health of vulnerable individuals (e.g., children, elderly, etc.). This study aimed to establish a new measuring platform and investigate PM emissions under four different ventilation conditions inside a car cabin without exposing any person to harmful tobacco smoke. Methods: PM concentrations were measured during the smoking of 3R4F reference cigarettes in a Mitsubishi Space Runner (interior volume 3.709 m3). The cigarettes were smoked with a machine, eliminating exposure of the researchers. Cigarettes were extinguished 4.5 min after ignition, and PM measurements continued until 10 min after ignition. Results: High mean PM concentrations were measured for cigarettes without ventilation after 4.5 min (PM10: 1150 µg/m3, PM2.5: 1132 µg/m3, PM1: 861.6 µg/m3) and after 10 min (PM10: 1608 µg/m3, PM2.5: 1583 µg/m3, PM1: 1133 µg/m3). 3R4F smoked under conditions with turned on ventilation resulted in reduction of PM compared to those smoked without ventilation after 4.5 min (PM10:-47.5 to -58.4%, PM2.5:-47.2 to -58%, PM1:-39.6 to -50.2%) and after 10 min (PM10:-70.8 to -74.4%, PM2.5:-70.6 to -74.3%, PM1:-64.0 to -68.0%). Cigarettes smoked without ventilation generated high PM peaks at 4.5 min (PM10: 2207 µg/m3, PM2.5: 2166 µg/m3, PM1: 1421 µg/m3) and at 10 min (PM10: 1989 µg/m3, PM2.5: 1959 µg/m3, PM1: 1375 µg/m3). PM peaks of cigarettes smoked under different ventilation modes varied at 4.5 min (PM10: 630-845 µg/m3, PM2.5: 625-836 µg/m3, PM1: 543 - 693 µg/m3) and 10 min (PM10: 124 - 130 µg/m3, PM2.5: 124 - 129 µg/m3, PM1: 118 - 124 µg/m3). Conclusion: The new measuring platform provides a safer way for researchers to investigate PM emissions of cigarettes. These data are comparable to published research and show that smoking in a parked vehicle with the windows closed generates harmful PM emissions even when the vehicle ventilation is in operation. Future studies should be carried out using the new measuring platform investigating PM exposure and PM distribution of in-vehicle smoking under a wide range of conditions. [ABSTRACT FROM AUTHOR]

Aim: The aim of this study was to estimate the percentage and sources of secondhand smoke (SHS) exposure among non-smoking pregnant women. It was a cross-sectional study conducted among the non-smoking pregnant women registered at the primary health center (PHC) under the All India Institute of Medical Science (AIIMS), Rishikesh. Materials and Methods: All registered pregnant women at sub-center in the field practice area (Raiwala) of the Department of Community and Family Medicine, AIIMS Rishikesh were recruited in the study. In this study, a questionnaire was used for measuring the exposure of SHS. Mean and standard deviation (SD), median, minimum, and maximum were used for continuous variables. A Chi-square test was used to compare the association of categorical variables. Results: Out of the total participants, 62% were exposed to SHS. 33% of participants were exposed to SHS at home only, 24% at public places only, and 5% were the ones exposed both at home and public places. More than half (69%) of the participants were having inadequate knowledge about the harms caused by SHS. Conclusions: More than half of the participants were exposed to SHS. Inadequate knowledge among the participants about adverse effects of SHS exposure and insufficient practices and action were observed. [ABSTRACT FROM AUTHOR]

Background: Allergic rhinitis (AR) is one of the most common allergic diseases affecting children. Objective assessment of nasal obstruction is possible through active anterior rhinomanometry (AAR). Several factors, such as passive smoke exposure (PSE), are triggers for worsening nasal obstruction and chronic inflammation. PSE affects bacterial eubiosis in the upper respiratory tract. This study evaluates the influence of PSE and cotinine levels on both nasal obstruction and local microbiome composition in children with AR. Methods: Fifty patients (aged between 6 and 16 years) with AR monosensitized grass pollen were enrolled. They underwent skin prick tests, a nasal swab to evaluate the microbial composition of the anterior nostrils, a basal AAR, a post‐decongestion AAR, and spirometry. Serum cotinine levels were assessed to evaluate PSE. Results: A significantly lower percentage of mean nasal flow (mNF%) was observed before and after hydrazine administration in subjects exposed to passive smoke (Exp group) compared with the non‐exposed group. In contrast, higher cotinine levels were observed in the Exp group than in the controls. PSE has been associated with a decrease in biodiversity and a change in the nasal microbiome composition; instead, although to a different extent, the abundance of specific taxa resulted in being correlated to cotinine levels and nasal flow. Conclusion: Children with AR exposed to passive smoke with positive serum cotinine could represent a risk factor for developing nasal obstruction and microbial dysbiosis, suggesting their possible role in pathophysiological processes. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study is to compare the gender‐different associations between secondhand smoke (SHS) exposure and diabetes in self‐reported never smokers verified by cotinine. Methods: Self‐reported never smokers verified by cotinine levels (<50 ng/mL) enrolled in the Kangbuk Samsung Health Study between April 2011 and December 2016 were included for this study. SHS exposure was defined as current exposure to passive smoke indoors at home or workplace. The gender‐specific association between SHS exposure and diabetes was assessed using multivariable regression analyses. Results: Of the total 131 724 individuals (mean age 35 years, SD 7.1 years), 66.8% were female, and the prevalence of SHS exposure in the entire population was 22.9%. The prevalence of diabetes in the group exposed to SHS was higher than that in the group unexposed to SHS only in females (1.8% vs 1.2%, P <.001 for females; 2.2% vs 2.2%, P =.956 for males). A significant gender interaction existed for the relationships between SHS exposure and diabetes (P for interaction <.001). The multivariate regression model showed that SHS exposure was significantly associated with diabetes only in females (odds ratio [95% CI], 1.40 [1.20, 1.65] for females; 1.00 [0.85, 1.19] for males). In particular, females with SHS exposure ≥1 hour/day, ≥3 times/week, and ≥10 years showed an increased risk of diabetes by more than 50% compared to those without SHS exposure. Conclusions: SHS exposure was significantly associated with diabetes in female never smokers with dose‐dependent relationship. However, further longitudinal studies are needed to elucidate the gender difference in the incidence of diabetes associated with SHS exposure. [ABSTRACT FROM AUTHOR]

Exposure to environmental tobacco smoke (ETS) is associated with high morbidity and mortality, mainly in childhood. Our aim was to evaluate the effects of postnatal ETS exposure in the brain 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) uptake of mice by positron emission tomography (PET) neuroimaging in a longitudinal study. C57BL/6J mice were exposed to ETS that was generated from 3R4F cigarettes from postnatal day 3 (P3) to P14. PET analyses were performed in male and female mice during infancy (P15), adolescence (P35), and adulthood (P65). We observed that ETS exposure decreased 18F-FDG uptake in the whole brain, both left and right hemispheres, and frontal cortex in both male and female infant mice, while female infant mice exposed to ETS showed decreased 18F-FDG uptake in the cerebellum. In addition, all mice showed reduced 18F-FDG uptake in infancy, compared to adulthood in all analyzed VOIs. In adulthood, ETS exposure during the early postnatal period decreased brain 18F-FDG uptake in adult male mice in the cortex, striatum, hippocampus, cingulate cortex, and thalamus when compared to control group. ETS induced an increase in 18F-FDG uptake in adult female mice when compared to control group in the brainstem and cingulate cortex. Moreover, male ETS-exposed animals showed decreased 18F-FDG uptake when compared to female ETS-exposed in the whole brain, brainstem, cortex, left amygdala, striatum, hippocampus, cingulate cortex, basal forebrain and septum, thalamus, hypothalamus, and midbrain. The present study shows that several brain regions are vulnerable to ETS exposure during the early postnatal period and these effects on 18F-FDG uptake are observed even a long time after the last exposure. This study corroborates our previous findings, strengthening the idea that exposure to tobacco smoke in a critical period interferes with brain development of mice from late infancy to early adulthood.

Exposure to environmental tobacco smoke (ETS) is associated with high morbidity and mortality, mainly in childhood. Our aim was to evaluate the effects of postnatal ETS exposure in the brain 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) uptake of mice by positron emission tomography (PET) neuroimaging in a longitudinal study. C57BL/6J mice were exposed to ETS that was generated from 3R4F cigarettes from postnatal day 3 (P3) to P14. PET analyses were performed in male and female mice during infancy (P15), adolescence (P35), and adulthood (P65). We observed that ETS exposure decreased 18F-FDG uptake in the whole brain, both left and right hemispheres, and frontal cortex in both male and female infant mice, while female infant mice exposed to ETS showed decreased 18F-FDG uptake in the cerebellum. In addition, all mice showed reduced 18F-FDG uptake in infancy, compared to adulthood in all analyzed VOIs. In adulthood, ETS exposure during the early postnatal period decreased brain 18F-FDG uptake in adult male mice in the cortex, striatum, hippocampus, cingulate cortex, and thalamus when compared to control group. ETS induced an increase in 18F-FDG uptake in adult female mice when compared to control group in the brainstem and cingulate cortex. Moreover, male ETS-exposed animals showed decreased 18F-FDG uptake when compared to female ETS-exposed in the whole brain, brainstem, cortex, left amygdala, striatum, hippocampus, cingulate cortex, basal forebrain and septum, thalamus, hypothalamus, and midbrain. The present study shows that several brain regions are vulnerable to ETS exposure during the early postnatal period and these effects on 18F-FDG uptake are observed even a long time after the last exposure. This study corroborates our previous findings, strengthening the idea that exposure to tobacco smoke in a critical period interferes with brain development of mice from late infancy to early adulthood. [ABSTRACT FROM AUTHOR]

Tobacco-free policy in Japan lags behind those of most developed countries. Evidence is required to promote strong implementation of existing policies. This study aimed to assess whether exposure to secondhand smoke (SHS) influences the incidence of streptococcal infection in young children, to further support the need for effective tobacco-free policies in Japan. This study used medical administrative claim and health check data from the Japan Health Insurance Association Fukuoka branch. Participants were beneficiaries' dependents younger than age 4 years. Exposure was defined as SHS from beneficiaries' smoking, each year during 2011–2014. The outcome was incidence of streptococcal infection, diagnosed with and without laboratory testing. Logistic regression analysis was performed to yield odds ratios (ORs) of associations with the outcome and 95% confidence intervals (CIs). This study included a total of 5743 children. The proportion of all participants with a record of streptococcal infection was 4.2% (n = 244). The results of logistic regression analysis between streptococcal infection and SHS exposure showed a significantly higher association (OR 1.39, 95% CI 1.07–1.80, P < 0.05) if all cases were included and an insignificant association with diagnoses using testing (OR 1.20, 95% Cl 0.80–1.80, P = 0.39). This study showed that 60% of streptococcal infections in young children were diagnosed without testing, and SHS increased this incidence regardless of testing. It reports new findings regarding the effect of SHS on infection in young children to support implementation and promotion of tobacco-free policies by the Japanese government not only in public spaces, but also at home. [ABSTRACT FROM AUTHOR]

In this study, we assessed trends of serum cotinine levels over time among US children ages 3–11 years and compared the risk of asthma in groups exposed to passive tobacco smoke. We utilized National Health and Nutrition Examination Survey (NHANES) data collected from 2003 to 2014 (n = 8064). Serum cotinine level, household smoker status, asthma status, and sociodemographic information were extracted for multiple regression analyses. The adjusted biannual change in log (cotinine) in comparison to earlier NHANES survey cycles was − 0.196 ( p  < 0.001) overall, − 0.055 ( p  = 0.089) among children with household smoker(s), and − 0.129 ( p  < 0.001) among children without. The proportion of children living with household smokers decreased from 24.9% in the 2003–2004 cycle to 11.4% in the 2013–2014 cycle. The adjusted odds ratios (ORs) for asthma were 1.34 (95% confidence interval (CI): 1.00–1.80; 2nd tertile vs 1st tertile) and 1.69 (95%CI: 1.25–2.29; 3rd tertile vs1st tertile), respectively. Highly exposed asthmatic children, in the 3rd cotinine tertile (>0.13 ng/mL), were primarily Non-Hispanic Black (61.0%) and whose family incomes were below poverty guidelines. Overall results reveal passive smoke exposure level among children ages 3–11 in the US decreased over the study period. Nevertheless, higher exposure to passive smoke is still associated with higher odds of childhood asthma. Targeted smoking cessation interventions in clinical practices are needed to reduce tobacco smoke exposure and related asthma risk in children, particularly in low-income and minority groups. [ABSTRACT FROM AUTHOR]

Limited human studies have investigated the impact of indoor air pollution on early childhood neurodevelopment among the US population. We aimed to examine the associations between prenatal and postnatal indoor air pollution exposure and early childhood development in a population-based birth cohort. This analysis included 4735 mother-child pairs enrolled between 2008 and 2010 in the Upstate KIDS Study. Indoor air pollution exposure from cooking fuels, heating fuels, and passive smoke during pregnancy, and at 12 and 36 months after birth were assessed by questionnaires. Five domains of child development were assessed by the Ages and Stages Questionnaire at 4, 8, 12, 18, 24, 30, and 36 months. Generalized estimating equations were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for potential confounders. Exposure to unclean cooking fuels (natural gas, propane, or wood) throughout the study period was associated with increased odds of failing any development domain (OR = 1.28, 95% CI 1.07, 1.53), the gross motor domain (OR = 1.52, 95% CI: 1.09, 2.13), and the personal-social domain (OR = 1.36, 95% CI: 1.00, 1.85), respectively. Passive smoke exposure throughout the study period increased the odds of failing the problem-solving domain by 71% (OR = 1.71, 95% CI 1.01, 2.91) among children of non-smoking mothers. No association was found between heating fuel use and failing any or specific domains. Unclean cooking fuel use and passive smoke exposure during pregnancy and early life were associated with developmental delays in this large prospective birth cohort. [Display omitted] • Unclean cooking fuel exposure was associated with failing developmental domains. • Passive smoke was associated with developmental delay in problem-solving skills. • There was no association of heating fuel use with failing any or specific domains. [ABSTRACT FROM AUTHOR]

Introduction Elevated levels of indoor air pollutants may cause cardiopulmonary disease such as lower respiratory infection, chronic obstructive lung disease and lung cancer, but the association with tuberculosis (TB) is unclear. So far the risk estimates of TB infection or/and disease due to indoor air pollution (IAP) exposure are based on self-reported exposures rather than direct measurements of IAP, and these exposures have not been validated. Objective The aim of this paper was to characterize and develop predictive models for concentrations of three air pollutants (PM 10 , NO 2 and SO 2 ) in homes of children participating in a childhood TB study. Methods Children younger than 15 years living within the eThekwini Municipality in South Africa were recruited for a childhood TB case control study. The homes of these children (n=246) were assessed using a walkthrough checklist, and in 114 of them monitoring of three indoor pollutants was also performed (sampling period: 24 h for PM 10 , and 2–3 weeks for NO 2 and SO 2 ). Linear regression models were used to predict PM 10 and NO 2 concentrations from household characteristics, and these models were validated using leave out one cross validation (LOOCV). SO 2 concentrations were not modeled as concentrations were very low. Results Mean indoor concentrations of PM 10 (n=105) , NO 2 (n=82) and SO 2 (n=82) were 64 μg/m 3 (range 6.6–241); 19 μg/m 3 (range 4.5–55) and 0.6 μg/m 3 (range 0.005–3.4) respectively with the distributions for all three pollutants being skewed to the right. Spearman correlations showed weak positive correlations between the three pollutants. The largest contributors to the PM 10 predictive model were type of housing structure (formal or informal), number of smokers in the household, and type of primary fuel used in the household. The NO 2 predictive model was influenced mostly by the primary fuel type and by distance from the major roadway. The coefficients of determination (R 2 ) for the models were 0.41 for PM 10 and 0.31 for NO 2 . Spearman correlations were significant between measured vs. predicted PM 10 and NO 2 with coefficients of 0.66 and 0.55 respectively. Conclusion Indoor PM 10 levels were relatively high in these households. Both PM 10 and NO 2 can be modeled with a reasonable validity and these predictive models can decrease the necessary number of direct measurements that are expensive and time consuming. [ABSTRACT FROM AUTHOR]

Objective: To investigate secondhand smoke exposure (SHS) of children at home and the prevalence of parental smoking after implementation of the new tobacco control law in Macao. This study explored whether the smoking ban in public places in Macao has decreased the prevalence of smoking or led to increased SHS exposure of children at home. As smokers cannot smoke in public places any more, they may smoke at home more frequently; a displacement effect of smoke-free legislation. Study design: Cross-sectional survey. Methods: This study surveyed 337 fathers and 538 mothers. Questions from a subset of key questions from the Global Adult Tobacco Survey (2nd edition) were applied to assess the SHS exposure of children and the prevalence of parental smoking since the smoking ban. A classification tree analysis was used to analyse the factors increasing SHS exposure of children. Results: The prevalence of SHS exposure in children at home was 41.3%. The prevalence rates of paternal and maternal smoking were 43.7% and 3.8%, respectively. Compared with data reported by the Health Bureau of Macao SAR in 2011, the prevalence of parental smoking and the prevalence of SHS exposure of children at home have not decreased since the smoking ban. Analysis of the factors increasing the prevalence of SHS exposure of children indicated that fathers with an education level below high school were more likely to contribute to this increase, compared with fathers with a high school education or more (48.2% vs 32.4%, respectively). In addition, fathers represented the majority of smokers at home, accounting for 92.0% of 415 smoking parents. The prevalence of paternal smoking (82.0%) in the group of children with SHS exposure was much higher than that in the unexposed group (16.7%, Chi-squared test = 367.199, P = 0.000). The SHS exposure of children increased consistently with the decrease in paternal education level. This was consistent with the increasing prevalence of paternal smoking as paternal education level decreased. SHS exposure was most common among children whose fathers had an education level below high school and whose mothers were aged ≤29 years (75.0%). Conclusions: This study did not find any decline in the prevalence of parental smoking after the smoking ban. These parents were more likely to smoke at home after the ban, leading to more frequent SHS exposure for their children. [ABSTRACT FROM AUTHOR]

Secondhand tobacco smoke is considered a developmental neurotoxicant especially given underdeveloped vital systems in young children. An ecological test of its negative influence on brain development can be made by examining the prospective association between early childhood household smoke exposure and later classroom behavior. Using a longitudinal birth cohort, we examined the unique contribution of household tobacco smoke exposure to children’s subsequent classroom engagement at age 10. From child ages 1.5 to 7 years, parents of 2,055 participants from the Quebec Longitudinal Study of Child Development reported on household smoking by themselves and other home occupants. At age 10, fourth-grade teachers reported on the child’s classroom engagement. In terms of prevalence, 58% of parents reported that their children were never exposed to smoke in the home, while 34% and 8% of children were exposed to transient and continuous household smoke, respectively. Compared with never exposed children, those who were exposed to transient and continuous household smoke scored 13% and 9% of a standard deviation lower on classroom engagement in fourth grade, standardized B = −.128 (95% confidence interval = −.186, −.069) and standardized B = −.093 (95% confidence interval = −.144, −.043), respectively. Compared with their never exposed peers, children exposed to transient and continuous early childhood household smoke showed proportionately less classroom engagement, which reflects task-orientation, following directions, and working well autonomously and with others. This predisposition poses risks for high school dropout, which from a population health perspective is closely linked with at-risk lifestyle habits and unhealthy outcomes. [ABSTRACT FROM AUTHOR]

Purpose To investigate the association of passive tobacco smoke exposure with early-onset myopia among three-year-old children in Singapore. Methods Pregnant mothers who attended their first trimester clinic at two major maternity units were recruited into the GUSTO birth cohort. The current analysis comprised 572 three-year-old children, who underwent cycloplegic autorefraction and axial length ( AL) measurements. Myopia was defined as spherical equivalent ( SE) of ≤−0.50 dioptres (D). Either parent completed questionnaires describing their child's exposure to passive smoke at six months, one and two years of age. Results There were 197 children (36.2%) who were exposed to passive smoke from birth to before six months. Compared to non-exposed children, children exposed to any passive smoke from birth to before six months experienced greater myopia prevalence (adjusted OR = 2.79; 95% CI: 1.24-6.29; p = 0.01). The odds of myopia in a child was greater if a smoker smokes at home, in the family car, or in the presence of the child (adjusted OR = 3.95; 95% CI: 1.41-11.09; p < 0.01) compared to non-exposed child. In contrast to myopia, childhood exposure to passive smoke did not systematically shift mean values for SE or AL. Conclusions In this prospective birth cohort study, we found that childhood exposure to passive smoke from birth to before six months slightly increased the risk of early-onset myopia. This may indicate a delayed response to passive smoke exposure before six months and the development of myopia at three years of age. Our study is limited by the small number of myopic children at this young age. Thus, larger prospective studies using more objective cotinine level measures are required to fully establish and understand the influence of tobacco smoke on refractive development in older children. [ABSTRACT FROM AUTHOR]

The adenoids are exposed to a wide number and variety of microbes, environmental pollutants, and food antigens. Atopy and passive smoke may significantly affect immune responses, mainly in children. The aim of the present study was to investigate whether passive exposure to tobacco smoke and/or atopy could affect immunoglobulin production by adenoidal lymphocytes in a cohort of children presenting with adenoid hypertrophy. A total of 277 children (151 males and 126 females; median age 5.5 years), with adenoidal hypertrophy requiring adenoidectomy and or adeno-tonsillectomy, were consecutively enrolled in the study. Adenoid mononuclear cells were in vitro stimulated with LPS or CpG. When considering both the presence of smoke exposure and atopy, we observed that the CpG-induced decrease in IgA and IgM production was significantly associated with this combination of risk factors. In the T-independent immunoglobulin production assay we found a positive association between the two risk factors and IgA and IgM production. In particular, the presence of both risk factors, showed a significant increase in IgA and IgM production after stimulation. In conclusion, this is the first study that investigated the in vitro adenoidal B cell response after different stimuli in children, also evaluating possible exposure to passive smoke and/or an atopic condition. [ABSTRACT FROM AUTHOR]

Individuals with Alpha-1 antitrypsin deficiency (AATD) have mutations in the SERPINA1 gene causing genetic susceptibility to early onset lung and liver disease that may result in premature death. Environmental interactions have a significant impact in determining the disease phenotype and outcome in AATD. The aim of this study was to assess the impact of smoke exposure on the clinical phenotype of AATD in Ireland. Clinical demographics and available thoracic computerised tomography (CT) imaging were detected from 139 PiZZ individuals identified from the Irish National AATD Registry. Clinical information was collected by questionnaire. Data was analysed to assess AATD disease severity and evaluate predictors of clinical phenotype. Questionnaires were collected from 107/139 (77%) and thoracic CT evaluation was available in 72/107 (67.2%). 74% of respondents had severe Chronic Obstructive Pulmonary Disease (COPD) (GOLD stage C or D). Cigarette smoking was the greatest predictor of impairment in FEV1 and DLCO (%predicted) and the extent of emphysema correlated most significantly with DLCO. Interestingly the rate of FEV1 decline was similar in ex-smokers when compared to never-smokers. Passive smoke exposure in childhood resulted in a greater total pack-year smoking history. Radiological evidence of bronchiectasis was a common finding and associated with increasing age. The Irish National AATD Registry facilitates clinical and basic science research of this condition in Ireland. This study illustrates the detrimental effect of smoke exposure on the clinical phenotype of AATD in Ireland and the benefit of immediate smoking cessation at any stage of lung disease. [ABSTRACT FROM AUTHOR]

Background: Prevalence of passive smoke exposure is relatively unknown in chronic rhinosinusitis (CRS). Previous studies have attempted to establish this relationship using subjective, questionnaire-based methodologies to assess smoke exposure, thus introducing the potential for error bias. The purpose of this study was to accurately determine the prevalence of passive smoke exposure in CRS and control patients using hair nicotine levels as a quantitative measure of cigarette smoke exposure. Methods: Hair samples were obtained at time of surgery from 569 patients: 404 undergoing surgery for CRS and 165 controls undergoing surgery for repair of cerebrospinal fluid leak, removal of pituitary tumors, or adenoidectomy from 2007 to 2013. Patient charts were reviewed for reported smoking status. Hair nicotine was quantified using reversed-phase high-performance liquid chromatography. Nonsmoking patients were classified as passive smoke exposed or smoke naïve according to the hair nicotine results. Statistical analysis was performed to test for differences in demographic information and smoke exposure prevalence between CRS, CRS subtypes, and controls. Results: The prevalence of passive smoke exposure in CRS as documented by hair nicotine was lower than previously reported subjective estimates. Passive smoke exposure rates were equivalent between those with CRS versus controls and significantly higher in children. Severity of passive smoke exposure was also equivalent between CRS subsets and controls. Annual passive smoke exposure prevalence did not change over time. Conclusion: There is no clear evidence of avoidance of passive smoke exposure in the CRS population compared with controls. Passive smoke exposure also remained stable over time despite recent regional implementation of smoking bans. Given the constancy of exposure, it is critical that the impact of passive smoke on CRS exacerbation, outcomes, and pathophysiology be evaluated in large-scale clinical studies. [ABSTRACT FROM AUTHOR]

Objectives To examine the association between time of smoking initiation and both the independent and joint effects of active and passive tobacco smoke exposure and the risk of breast cancer in a sample of Ontario women. Methods Data from two large population-based case-control studies conducted among Ontario women aged 25–75 years were combined for analysis (n = 12,768). Results Women who had ever smoked and were exposed to passive smoke had a significant increased risk of breast cancer (OR 1.13, 95%CI 1.01–1.25). A significant increased risk was also observed among women who initiated smoking: at age 26 or older (OR 1.26, 95%CI 1.03–1.55); more than five years from menarche (OR 1.26, 95%CI 1.12–1.42); and, after their first live birth (OR 1.25, 95%CI 1.02–1.52). Conclusions The results suggest that women who initiate smoking at an older age are at an increased risk of breast cancer.

Background: It is well recognized that genetic variation as well as environmental factors modulates breast cancer risk. Deficiencies in DNA repair capacity are thought to associate with breast cancer risk. The main aim of this study was to use the mutagen sensitivity assay as an indirect measure of DNA repair capacity to assess breast cancer risk and the relationship between passive smoking and breast cancer risk among women in China. Methods: We carried out a case-control study, involving 196 Chinese patients with breast cancer and 211 controls without the disease and with no history of cancer. We investigated the association between mutagen sensitivity and breast cancer risk using bleomycin as the mutagen. Mutagen sensitivity was measured by quantifying the chromatid breaks induced by mutagens in short-term cultures of peripheral blood lymphocytes. Nonparametric tests and the Fisher's exact test were used to determine the statistical significance of the crude case-control comparisons, followed by logistic regression to adjust for important covariates. Results: The mean number of bleomycin-induced breaks per cell was 0.81 for cases compared with 0.73 for the controls ( p = 0.016). A greater number of bleomycin-induced chromosomal breaks per cell was associated with an increased risk of breast cancer (adjusted odds ratio of 1.82, p trend <0.01). The association between bleomycin sensitivity and breast cancer risk was greater for women who were exposed to tobacco smoke (passive smokers). The combination of bleomycin sensitivity and exposure to tobacco smoke increased risk further; women passive smokers with high sensitivity to bleomycin had a 2.77-fold increased risk of breast cancer. Conclusions: Our data indicate that increased bleomycin-induced mutagen sensitivity is significantly associated with an increased risk of breast cancer among Chinese women. Exposure to passive smoke is also associated with increased breast cancer risk, and the correlation is even greater for women with both longer passive exposure to tobacco smoke and high sensitivity to bleomycin. [ABSTRACT FROM AUTHOR]

Aims To examine whether English legislation to make virtually all indoor public places and work-places smoke-free on 1 July 2007 displaced smoking into the home and hence increased the proportion of children exposed to levels of second-hand smoke known to be detrimental to health. Design Repeated cross-sectional study with data from 10 annual surveys undertaken from 1996 to 2008. Setting England. Participants Nationally representative samples of non-smoking children aged 4-15 years old living in private households. Measurements Salivary cotinine, parental smoking status, whether smoking is allowed within the house, socio-demographic variables. Findings The proportion of children exposed to damaging levels of second-hand smoke (defined as those with cotinine levels >1.7 ng/ml) has fallen over time, from 23.5% in 1996 to 12.6% in 2008. The legislation was not associated with further changes in the proportion of children above this threshold-the odds of having cotinine >1.7 ng/ml did not change after adjustment for the pre-legislative trend and confounders (odds ratio: 1.0, 95% confidence interval: 0.78, 1.4). Non-significant associations were also found when examining children by parental or household smoking status. Conclusions Legislation to prohibit smoking in indoor public places and work-places does not increase the proportion of children exposed to damaging levels of second-hand smoke. Even in a country with a strong tobacco control climate, a significant proportion of children remain highly exposed to second-hand smoke and future policies need to include interventions to reduce exposure among these children. [ABSTRACT FROM AUTHOR]

Background: On 1 July 2007, smokefree legislation was implemented in England, which made virtually all enclosed public places and workplaces smokefree. Objectives: We examined trends in and predictors of secondhand smoke exposure among nonsmoking adults to determine whether exposure changed after the introduction of smokefree legislation and whether these changes varied by socioeconomic status (SES) and by household smoking status. Methods: We analyzed salivary cotinine data from the Health Survey for England that were collected in 7 of 11 annual surveys undertaken between 1998 and 2008. We conducted multivariate regression analyses to examine secondhand smoke exposure as measured by the proportion of nonsmokers with undetectable levels of cotinine and by geometric mean cotinine. Results: Secondhand smoke exposure was higher among those exposed at home and among lower-SES groups. Exposure declined markedly from 1998 to 2008 (the proportion of participants with undetectable cotinine was 2.9 times higher in the last 6 months of 2008 compared with the first 6 months of 1998 and geometric mean cotinine declined by 80%). We observed a significant fall in exposure after legislation was introduced-the odds of having undetectable cotinine were 1.5 times higher [95% confidence interval (CI): 1.3, 1.8] and geometric mean cotinine fell by 27% (95% CI: 17%, 36%) after adjusting for the prelegislative trend and potential confounders. Significant reductions were not, however, seen in those living in lower-social class households or homes where smoking occurs inside on most days. Conclusions: We found that the impact of England's smokefree legislation on secondhand smoke exposure was above and beyond the underlying long-term decline in secondhand smoke exposure and demonstrates the positive effect of the legislation. Nevertheless, some population subgroups appear not to have benefitted significantly from the legislation. This finding suggests that these groups should receive more support to reduce their exposure. [ABSTRACT FROM AUTHOR]

The article discusses a study to evaluate the relationship between father's smoking status during pregnancy, and neonatal and maternal salivary cotinine immediately after delivery, and evaluate the potential use of salivary cotinine measurements immediately after birth to determine exposure of neonates to passive smoke. The study concluded that smoking indoors by the father affected the mother and neonate and that salivary cotinine measurement is good to evaluate passive smoking exposure.

Objectives: The aim of this study was to examine the association between objectively measured secondhand smoke (SHS) exposure and incident cardiovascular disease (CVD) death and assess the extent to which this association can be explained through novel circulating markers of inflammation and hemostasis. Background: Existing evidence suggests there is an association between SHS and CVD risk, although the mechanisms remain poorly understood. Methods: In a prospective study of 13,443 participants living in England and Scotland (age 53.5 ± 12.6 years, 52.3% women), we measured salivary cotinine (an objective marker of SHS exposure) and novel CVD biomarkers (C-reactive protein, fibrinogen) at baseline. Results: Of the sample, 20.8% had high SHS exposure on the basis of elevated levels of salivary cotinine (range 0.71 to 14.99 ng/ml). During a mean follow-up of 8 years, there were 1,221 all-cause deaths and 364 CVD deaths. High SHS was associated with all-cause (age-adjusted hazard ratio [HR]: 1.25, 95% confidence interval [CI]: 1.02 to 1.53) and CVD death (age-adjusted HR: 1.21, 95% CI: 0.85 to 1.73). High SHS was also associated with elevated CRP, which explained 48% of the association between SHS and CVD death. The excess risk of CVD associated with active smoking was exaggerated in relation to self report (age-adjusted HR: 3.27, 95% CI: 2.48 to 4.31) compared with objective assessment (age-adjusted HR: 2.44, 95% CI: 1.75 to 3.40). Conclusions: Among a large representative sample of British adults we observed elevated levels of low-grade inflammation in otherwise healthy participants exposed to high SHS, and this partly explained their elevated risk of CVD death. [Copyright &y& Elsevier]

Smoking is associated with multiple adverse pregnancy outcomes, including fetal growth restriction. The objective of this study was to determine whether cigarette smoke exposure during pregnancy in a mouse model affects the functional properties of maternal uterine, mesenteric, and renal arteries as a possible mechanism for growth restriction. C57B1/CJ mice were exposed to whole body sidestream smoke for 4 h/day. Smoke particle exposure was increased from day 4 of gestation until late pregnancy (day /6-19), with mean total suspended particle levels of 63 mg/rn3, representative of moderate-to-heavy smoking in humans. Uterine, mesenteric, and renal arteries from late-pregnant and virgin mice were isolated and studied in a pressure-arteriograph system (a = 23). Plasma cotinine was measured by ELISA. Fetal weights were significantly reduced in smoke-exposed compared with control fetuses (0.88 ± 0.1 vs. 1.0 ± 0.08 g, P < 0.02), while litter sizes were not different. Endothelium-mediated relaxation responses to methacholine were significantly impaired in both the uterine and mesenteric vasculature of pregnant mice exposed to cigarette smoke during gestation. This difference was not apparent in isolated renal arteries from pregnant mice exposed to cigarette smoke; however, relaxation was significantly reduced in renal arteries from smoke-exposed virgin mice. In conclusion, we found that passive cigarette smoke exposure is associated with impaired vascular relaxation of uterine and mesenteric arteries in pregnant mice. Functional maternal vascular perturbations during pregnancy, specifically impaired peripheral and uterine vasodilation, may contribute to a mechanism by which smoking results in fetal growth restriction. [ABSTRACT FROM AUTHOR]

1,3-Butadiene and acrylonitrile are important industrial chemicals that have a high production volume and are ubiquitous environmental pollutants. The urinary mercapturic acids of 1,3-butadiene and acrylonitrile— N-acetyl- S-(3,4-dihydroxybutyl)cysteine (DHBMA) and MHBMA (an isomeric mixture of N-acetyl- S-((1-hydroxymethyl)-2-propenyl)cysteine and N-acetyl- S-((2-hydroxymethyl)-3-propenyl)cysteine) for the former and N-acetyl- S-2-cyanoethylcysteine (CEMA) for the latter—are specific biomarkers for the determination of individual internal exposure to these chemicals. We have developed and validated a fast, specific, and very sensitive method for the simultaneous determination of DHBMA, MHBMA, and CEMA in human urine using an automated multidimensional LC/MS/MS method that requires no additional sample preparation. Analytes are stripped from urinary matrix by online extraction on a restricted access material, transferred to the analytical column, and subsequently determined by tandem mass spectrometry using labeled internal standards. The limits of quantification (LOQs) for DHBMA, MHBMA, and CEMA were 10 µg/L, 2 µg/L, and 1 µg/L urine, respectively, and were sufficient to quantify the background exposure of the general population. Precision within series and between series for all analytes ranged from 5.4 to 9.9%; mean accuracy was between 95 and 115%. We applied the method on spot urine samples from 210 subjects from the general population with no occupational exposure to 1,3-butadiene or acrylonitrile. A background exposure of the general population to acrylonitrile was discovered that is basically influenced by individual exposure to passive smoke as well as active smoking habits. Smokers showed a significantly higher excretion of MHBMA, whereas DHBMA levels did not differ significantly. Owing to its automation, our method is well suited for application in occupational or environmental studies. [Figure not available: see fulltext.] [ABSTRACT FROM AUTHOR]

Purpose: The present investigation prospectively examined active cigarette smoking and household passive smoke exposure and the risk of developing rectal cancer. Methods: Cigarette smoking data were collected on all household members during two private censuses in Washington County, Maryland. These two cohorts were followed up, one cohort from 1963–1978 and the other from 1975–1994 for first-time diagnoses of rectal cancer. We identified 148 and 169 rectal cancer cases in the 1963 and 1975 cohorts, respectively. Relative risks were estimated by means of Poisson regression models. Results: In men, the adjusted relative risks (aRR) and 95% confidence intervals (CI) for the association between current smoking and rectal cancer were 3.1 (1.2–7.8) in the 1963 cohort and 1.8 (0.9–3.7) in the 1975 cohort; the corresponding aRRs in women were 0.9 (0.5–1.8) and 1.6 (0.9–3.8) in the 1963 and 1975 cohorts, respectively. In nonsmokers, household passive smoke exposure was strongly associated with rectal cancer among men in the 1963 cohort (aRR = 5.8; 1.8–18.4) but not the 1975 cohort (aRR = 1.1; 0.2–5.0). In women, household passive exposure was not strongly associated with rectal cancer in either cohort. Conclusions: The results of our study suggest that active cigarette smoking may contribute to rectal cancer risk, but inconsistencies in the findings preclude drawing strong, clear-cut inferences. [Copyright &y& Elsevier]

Daily personal exposures to benzo(a)pyrene (BaP) of 31 newsagents working in Genoa, Italy, were evaluated throughout 1998 during two different seasonal periods (February–April and May–June). Exposures of smoker and non-smoker subjects were compared.The highest BaP exposures were those of smokers during the cold period (2.20±0.84 ng/m3). During this same period, the BaP exposure for non-smoker subjects was 1.00±0.32 ng/m3. Both smoker and non-smoker exposures showed a seasonal dependence, with the lowest values occurring in the warm period (smokers: 1.46±0.72 ng/m3, non-smokers: 0.65±0.25 ng/m3). Compared to the cold period, the warm period produced a nearly 35% reduction in BaP exposures in both smoker and non-smoker subjects.A linear correlation was observed between personal exposures and number of cigarettes smoked daily. An increase in average daily BaP exposure of 0.071±0.009 ng/m3 for every cigarette, due to passive smoke, was calculated.Mean BaP concentrations calculated from fixed monitoring stations were nearly 40% higher than mean personal exposures of non-smoker newsagents. [Copyright &y& Elsevier]

Private-label cigarettes are cigarettes that belong to the retailer itself. Private-label cigarettes from discounters or supermarkets are cheaper than brand-name cigarettes, and their lower price has allowed them to garner an ever-increasing share of the tobacco product market, especially among lower socioeconomic groups. Particulate matter (PM), a considerable component of air pollution, is a substantial health-damaging factor. Smoking is the primary source of PM in smokers’ homes. In a 2.88 m3 measuring chamber, the PM emission fractions PM10, PM2.5, and PM1 from three private-label cigarette brands and three brand-name cigarette brands with identical nicotine, tar, and carbon monoxide content were measured and compared to those of a reference cigarette by laser aerosol spectroscopy. All cigarette brands emitted PM in health-threatening quantities. The measurement results ranged from 1394 µg/m3 to 1686 µg/m3 PM10, 1392 µg/m3 to 1682 µg/m3 PM2.5, and 1355 µg/m3 to 1634 µg/m3 PM1, respectively. Only one private-label brand differed significantly (p < 0.001) from the other cigarette brands, which were tested with slightly lower PM levels. All other brands differed only marginally (not significant, p > 0.05) from one another. Significant (p < 0.05) negative correlations between private-label and brand-name cigarettes were found for PM10, PM2.5, and PM1 when accounting for tobacco filling densities, and for PM1 when accounting for filter lengths. The especially health-hazardous fraction PM1 accounted for the largest proportion of PM emissions from the cigarettes tested. The results of this study suggest that- cheaper tobacco products are as harmful as more expensive ones, at least regarding PM emissions. This highlights the importance of anti-smoking campaigns, especially for lower socioeconomic groups, where smoking is more widespread. Governments should reduce the price gap between cheap and more expensive tobacco products by implementing specific tobacco taxes. In such a case, at increasing prices of tobacco products, a downward shift to private-label cigarettes would probably decrease.