Abstract:In-home SHS exposure remains alarmingly high in urban environments. However, a substantial proportion of this exposure appears to be occurring only from external sources that enter the home. Caregivers in these homes had higher desire but lower agency to avoid SHSe, driven by lack of functional support and physical isolation. Public policies targeting these factors may help remediate exposure in this especially vulnerable population.
“…43 Children living in US urban centers are at risk for secondhand smoke exposure as multiple studies have found ≥50% of urban children are exposed to SHS. 10,[44][45][46] This percentage is higher than expected, as currently 12.4% of US adults and 8.1% of US adolescents are active smokers, 47 illustrating both higher rates of tobacco use and overcrowding in urban households. Moreover, persons living in poverty, children under age 11, non-Hispanic Blacks, persons living in rental housing, and those with less than a high school education are more likely to be exposed to SHS.…”
Section: Indoor and Outdoor Urban P Ollutantsmentioning
confidence: 99%
“…Children living in US urban centers are at risk for secondhand smoke exposure as multiple studies have found ≥50% of urban children are exposed to SHS 10,44–46 47 illustrating both higher rates of tobacco use and overcrowding in urban households.…”
Section: Indoor and Outdoor Urban Pollutantsmentioning
Children with asthma who live in urban neighborhoods experience a disproportionately high asthma burden, with increased incident asthma and increased asthma symptoms, exacerbations, and acute visits and hospitalizations for asthma. There are multiple urban exposures that contribute to pediatric asthma morbidity, including exposure to pest allergens, mold, endotoxin, and indoor and outdoor air pollution. Children living in urban neighborhoods also experience inequities in social determinants of health, such as increased poverty, substandard housing quality, increased rates of obesity, and increased chronic stress. These disparities then in turn can increase the risk of urban exposures and compound asthma morbidity as poor housing repair is a risk factor for pest infestation and mold exposure and poverty is a risk factor for exposure to air pollution. Environmental interventions to reduce in‐home allergen concentrations have yielded inconsistent results. Population‐level interventions including smoking bans in public places and legislation to decrease traffic‐related air pollution have been successful at reducing asthma morbidity and improving lung function growth. Given the interface and synergy between urban exposures and social determinants of health, it is likely population and community‐level changes will be needed to decrease the excess asthma burden in children living in urban neighborhoods.
“…43 Children living in US urban centers are at risk for secondhand smoke exposure as multiple studies have found ≥50% of urban children are exposed to SHS. 10,[44][45][46] This percentage is higher than expected, as currently 12.4% of US adults and 8.1% of US adolescents are active smokers, 47 illustrating both higher rates of tobacco use and overcrowding in urban households. Moreover, persons living in poverty, children under age 11, non-Hispanic Blacks, persons living in rental housing, and those with less than a high school education are more likely to be exposed to SHS.…”
Section: Indoor and Outdoor Urban P Ollutantsmentioning
confidence: 99%
“…Children living in US urban centers are at risk for secondhand smoke exposure as multiple studies have found ≥50% of urban children are exposed to SHS 10,44–46 47 illustrating both higher rates of tobacco use and overcrowding in urban households.…”
Section: Indoor and Outdoor Urban Pollutantsmentioning
Children with asthma who live in urban neighborhoods experience a disproportionately high asthma burden, with increased incident asthma and increased asthma symptoms, exacerbations, and acute visits and hospitalizations for asthma. There are multiple urban exposures that contribute to pediatric asthma morbidity, including exposure to pest allergens, mold, endotoxin, and indoor and outdoor air pollution. Children living in urban neighborhoods also experience inequities in social determinants of health, such as increased poverty, substandard housing quality, increased rates of obesity, and increased chronic stress. These disparities then in turn can increase the risk of urban exposures and compound asthma morbidity as poor housing repair is a risk factor for pest infestation and mold exposure and poverty is a risk factor for exposure to air pollution. Environmental interventions to reduce in‐home allergen concentrations have yielded inconsistent results. Population‐level interventions including smoking bans in public places and legislation to decrease traffic‐related air pollution have been successful at reducing asthma morbidity and improving lung function growth. Given the interface and synergy between urban exposures and social determinants of health, it is likely population and community‐level changes will be needed to decrease the excess asthma burden in children living in urban neighborhoods.
“…Starting from this evidence, in the present study, we analysed NGF and its receptors in a group of non-smokers, adult volunteers exposed to short-term SS in a controlled home-like environment [ 27 , 44 ]. Determination of cotinine levels in urine samples was used as the classical, standard biomarker of SS exposure, as described in the literature [ 31 , 45 ].…”
Environmental tobacco smoke remains a major risk factor, for both smokers and non-smokers, able to trigger the initiation and/or the progression of several human diseases. Although in recent times governments have acted with the aim of banning or strongly reducing its impact within public places and common spaces, environmental tobacco smoke remains a major pollutant in private places, such as the home environment or cars. Several inflammatory and long-term biomarkers have been analysed and well-described, but the list of mediators modulated during the early phases of inhalation of environmental tobacco smoke needs to be expanded. The aim of this study was to measure the short-term effects after exposure to side-stream smoke on Nerve Growth Factor and its receptors Tropomyosin-related kinase A and neurotrophin p75, molecules already described in health conditions and respiratory diseases. Twenty-one non-smokers were exposed to a home-standardized level of SS as well as to control smoke-free air. Nerve Growth Factor and inflammatory cytokines levels, as well the expression of Tropomyosin-related kinase A and neurotrophin receptor p75, were analysed in white blood cells. The present study demonstrates that during early phases, side-stream smoke exposure induced increases in the percentage of neurotrophin receptor p75-positive white blood cells, in their mean fluorescent intensity, and in gene expression. In addition, we found a positive correlation between the urine cotinine level and the percentage of neurotrophin receptor-positive white blood cells. For the first time, the evidence that short-term exposure to side-stream smoke is able to increase neurotrophin receptor p75 expression confirms the very early involvement of this receptor, not only among active smokers but also among non-smokers exposed to SS. Furthermore, the correlation between cotinine levels in urine and the increase in neurotrophin receptor p75-positive white blood cells could represent a potential novel molecule to be investigated for the detection of SS exposure at early time points.
“…Air nicotine concentration can be measured to assess SHS exposure in a specific environment [12]. Nicotine is specific to tobacco smoke and often used to evaluate SHS in different indoor settings [13][14][15]. The biomarker cotinine, a nicotine metabolite, can be used to determine individual SHS exposure.…”
Objective
This study was conducted to describe secondhand smoke (SHS) exposure among non-smoking employees in the workplace, and identify factors related to SHS exposure in Qingdao.
Methods
The study participants covered key non-smoking places stipulated in the “Qingdao City Smoking Control Regulations,” which included three categories: restaurants, bars, and office buildings. Airborne nicotine concentration in the workplace and saliva cotinine concentration of employees were measured. The questionnaire included employees’ demographic factors, smoke-free measures in the workplace, employers’ tobacco hazard knowledge, and attitudes towards smoke-free policy.
Results
A total of 222 non-smoking employees and 46 non-smoking employers were included in the study. The median concentrations of airborne nicotine and salivary cotinine were 0.389 μg/m3 and 0.575 ng/mL, respectively. Educational status, average number of workplace smokers per day, exposure time to SHS in the workplace, and whether smoking and non-smoking areas were divided significantly related to airborne nicotine concentration. Age, educational status, exposure time to SHS in the workplace, tobacco control training and publicity, and whether the employers support the “Qingdao Tobacco Control Regulation” were significantly related to salivary cotinine concentration.
Conclusions
Despite the implementation of the “Qingdao Smoking Control Regulations” in 2013, the workplace remains an important location for SHS exposure. Interventions such as raising workers’ awareness of the risks associated with SHS exposure through health education and developing smoking prevention and cessation programs to reduce SHS exposure in the workplace are urgently needed.
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