Environmental Cigarette Smoke Research Articles

Fertility loss: negative effects of environmental toxicants on oogenesis.

There has been a global decline in fertility rates, with ovulatory disorders emerging as the leading cause, contributing to a global lifetime infertility prevalence of 17.5%. Formation of the primordial follicle pool during early and further development of oocytes after puberty is crucial in determining female fertility and reproductive quality. However, the increasing exposure to environmental toxins (through occupational exposure and ubiquitous chemicals) in daily life is a growing concern; these toxins have been identified as significant risk factors for oogenesis in women. In light of this concern, this review aims to enhance our understanding of female reproductive system diseases and their implications. Specifically, we summarized and categorized the environmental toxins that can affect oogenesis. Here, we provide an overview of oogenesis, highlighting specific stages that may be susceptible to the influence of environmental toxins. Furthermore, we discuss the genetic and molecular mechanisms by which various environmental toxins, including metals, cigarette smoke, and agricultural and industrial toxins, affect female oogenesis. Raising awareness about the potential risks associated with toxin exposure is crucial. However, further research is needed to fully comprehend the mechanisms underlying these effects, including the identification of biomarkers to assess exposure levels and predict reproductive outcomes. By providing a comprehensive overview, this review aims to contribute to a better understanding of the impact of environmental toxins on female oogenesis and guide future research in this field.

The Burden of Diseases From Exposure to Environmental Cigarette Smoke: A Case Study of Municipal Staff in Qazvin, Iran

This study aimed to estimate the burden of diseases (BoD) from environmental cigarette smoke (ECS) exposure. More precisely, the study examined the prevalence of non-communicable diseases (NCDs) related to cigarette smoking in municipal staff based on a prospective cohort study. This cross-sectional study was designed among municipal employees, aged 25-55 years in Qazvin, Iran during 2019-2020. The data on cigarette smoking and environmental exposure were obtained using a standard questionnaire. Finally, systolic blood pressure (SBP) and diastolic blood pressure (DBP), fasting blood sugar (FBS), triglyceride (TG), high-density lipoprotein, and low-density lipoprotein were measured to assess the relation between active cigarette smoking and the prevalence of NCDs, including hypertension and diabetes in workers. The prevalence of cigarette smoking was 16.2%. In addition, 15% of staff were exposed to ECS. The prevalence of anemia and high TG levels in current cigarette smokers was 2.71 (P=0.024) and 1.4 times higher than among non-smokers (P=0.027). The total number of disability-adjusted life years (DALYs) caused by lung cancer, asthma, and ischemic heart disease (IHD) attributable to ECS was 0.65 per 1000 adults annually. Further, the number of 0.058 death was estimated per 1000 adults annually at the workplace. Most deaths were caused by IHD (79%), followed by lung cancer (12%) and asthma (9%). It was revealed that the number of DALYs and deaths attributable to secondhand smoke (SHS) was 0.34 and 0.3 vs. 0.028 and 0.029 per 1000 adults in men and women, respectively. The results demonstrated that exposure to ECS is an important factor in increasing the risk of the prevalence of NCDs and can increase the BoD attributable to cigarette smoking.

Pandemic COVID-19 and environmental pollution (literature review)

The purpose of this article is to review and analyze the literature on the impact of the COVID-19 pandemic on the environment and, conversely, on the environmental impact on the spread of SARS-CoV-2. The literature search was carried out using the MedLine, PubMed and eLIBRARY databases. Thanks to measures to combat the COVID-19 pandemic, the world experienced a sharp decline in economic activity, which in turn led to improvements in air and water quality and contributed to the global reduction in greenhouse gas emissions, but this improvement was short-lived. Quarantine measures not only protect the population from COVID-19, but also positively affect the environmental quality. At the same time, the amount of plastic medical waste, such as used public and personal protective equipment against COVID-19, increased, and as a result, the problem of their disposal arose. This has led to the contamination of the water and land physical spaces and created the population contamination threat. Using the concentration of SARS-CoV-2 RNA from urban wastewater and subsequent counting of viral RNAs by quantitative reverse transcriptase polymerase chain reaction, an early determination of COVID-19 was carried out by modelling in specific populations. The presence of SARS-CoV-2 RNA in wastewater is a potential public health risk. High levels of environmental pollution (long-term exposure to derivatives of fossil fuel combustion), meteorological parameters (ionizing and UV radiation), and cigarette smoke, are considered to be additional factors increasing the spread and mortality of COVID-19. The SARS-CoV-2 viability depends on aquatic and terrestrial environmental parameters.

Use of urinary cotinine and cotinine/creatinine ratio as a biomarker of environmental tobacco exposure

Purpose: Exposure to Environmental Tobacco Smoke (ETS) remains a worldwide public health problem. The purpose of this study was to investigate the relationship between parents' smoking habits at home and children's exposure to environmental tobacco smoke by measuring urinary cotinine levels and urine cotinine/creatinine ratios in children.
 Materials and Methods: This case-control typed analytical study was conducted with 357 children in the 0-18 age group. The case group consisted of 180 children exposed to environmental cigarette smoke. As the control group, it consisted of 177 healthy children and non-smoking in their family. The levels of cotinine and creatinine in spot urinary were analyzed in both groups.
 Results: The urinary cotinine level of the children was found to be statistically higher in those whose parents were smokers, female gender, fathers with a low educational level, and those with 3 or fewer rooms in the house. The urinary cotinine/creatinine ratio of the children was found to be statistically higher in those whose parents were smokers (15.91 pg/mg (1.54-147.54) vs 7.90 pg/mg (1.29-68.52)), female gender (13.19 pg/mg (1.79-115.07) vs 10.45 pg/mg (1.29-147.54)). Urinary cotinine levels in the ETS exposed group were affected 1042 times more than in the ETS unexposed group [OR:1042,462, 95% CI (139.821.839-7772.246)]. 
 Conclusion: In the present study, urinary cotinine levels were found to be higher in children exposed to tobacco smoke than in children not exposed to tobacco smoke. In the light of these results, urinary cotinine can be used as a biomarker to evaluate exposure to ETS in children. Educating parents is essential to raising their awareness of exposure to ETS and teaching the right behaviors to protect children's health, especially in the home environment.

Prenatal and Postnatal Cigarette Smoke Exposure Is Associated With Increased Risk of Exacerbated Allergic Airway Immune Responses: A Preclinical Mouse Model

Increased exposure to household air pollution and ambient air pollution has become one of the world’s major environmental health threats. In developing and developed countries, environmental cigarette smoke (CS) exposure is one of the main sources of household air pollution (HAP). Moreover, results from different epidemiological and experimental studies indicate that there is a strong association between HAP, specifically CS exposure, and the development of allergic diseases that often persists into later life. Here, we investigated the impact of prenatal and postnatal CS exposure on offspring susceptibility to the development of allergic airway responses by using a preclinical mouse model. Pregnant BALB/c mice were exposed to either CS or air during pregnancy and lactation and in order to induce allergic asthma the offspring were sensitized and challenged with house dust mite (HDM). Decreased lung function parameters, like dynamic compliance and pleural pressure, were observed in PBS-treated offspring born to CS-exposed mothers compared to offspring from air-exposed mothers. Maternal CS exposure significantly increased the HDM-induced airway eosinophilia and neutrophilia in the offspring. Prenatal and postnatal CS exposure increased the frequency of Th2 cells in the lungs of HDM-treated offspring compared to offspring born to air-exposed mothers. Offspring born to CS-exposed mothers showed increased levels of IL-4, IL-5 and IL-13 in bronchoalveolar lavage fluid compared to offspring from air-exposed mothers. Ex-vivo restimulation of lung cells isolated from HDM-treated offspring born to CS-exposed mothers also resulted in increased IL-4 production. Finally, serum immunoglobulins levels of HDM-specific IgE and HDM-specific IgG1 were significantly increased upon a HDM challenge in offspring born to CS-exposed mothers compared to offspring from air-exposed mothers. In summary, our results reveal a biological plausibility for the epidemiological studies indicating that prenatal and postnatal CS exposure increases the susceptibility of offspring to allergic immune responses.

Paternal metabolic and cardiovascular programming of their offspring: A systematic scoping review.

BackgroundThere is lots of evidence that maternal peri-gestational metabolic, genomic and environmental conditions are closely linked to metabolic and cardiovascular outcomes in their offspring later in life. Moreover, there is also lotsof evidence that underlining mechanisms, such as molecular as well as epigenetic changes may alter the intrauterine environment leading to cardio-metabolic diseases in their offspring postnatal. But, there is also increasing evidence that cardio-metabolic diseases may be closely linked to their paternal metabolic risk factors, such as obesity, Type 2 Diabetes and other risk factors.ObjectiveTo analyse the evidence as well as specific risk factors of paternal trans-generational programming of cardio-metabolic diseases in their offspring.MethodsWithin a systematic scoping review, we performed a literature search in MEDLINE (PubMed) and EMBASE databases in August 2020 considering original research articles (2000–2020) that examined the impact of paternal programming on metabolic and cardiovascular offspring health. Epidemiological, clinical and experimental studies as well as human and animal model studies were included.ResultsFrom n = 3.199 citations, n = 66 eligible studies were included. We selected n = 45 epidemiological as well as clinical studies and n = 21 experimental studies. In brief, pre-conceptional paternal risk factors, such as obesity, own birth weight, high-fat and low-protein diet, undernutrition, diabetes mellitus, hyperglycaemia, advanced age, smoking as well as environmental chemical exposure affect clearly metabolic and cardiovascular health of their offspring later in life.ConclusionsThere is emerging evidence that paternal risk factors, such as paternal obesity, diabetes mellitus, nutritional habits, advanced age and exposure to environmental chemicals or cigarette smoke, are clearly associated with adverse effects in metabolic and cardiovascular health in their offspring. Compared to maternal programming, pre-conceptional paternal factors might also have also a substantial effect in the sense of trans-generational programming of their offspring and need further research.

Inhalation exposure to cigarette smoke and inflammatory agents induces epigenetic changes in the lung

Smoking-related lung tumors are characterized by profound epigenetic changes including scrambled patterns of DNA methylation, deregulated histone acetylation, altered gene expression levels, distorted microRNA profiles, and a global loss of cytosine hydroxymethylation marks. Here, we employed an enhanced version of bisulfite sequencing (RRBS/oxRRBS) followed by next generation sequencing to separately map DNA epigenetic marks 5-methyl-dC and 5-hydroxymethyl-dC in genomic DNA isolated from lungs of A/J mice exposed whole-body to environmental cigarette smoke for 10 weeks. Exposure to cigarette smoke significantly affected the patterns of cytosine methylation and hydroxymethylation in the lungs. Differentially hydroxymethylated regions were associated with inflammatory response/disease, organismal injury, and respiratory diseases and were involved in regulation of cellular development, function, growth, and proliferation. To identify epigenetic changes in the lung associated with exposure to tobacco carcinogens and inflammation, A/J mice were intranasally treated with the tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), the inflammatory agent lipopolysaccharide (LPS), or both. NNK alone caused minimal epigenetic alterations, while exposure either to LPS or NNK/LPS in combination led to increased levels of global cytosine methylation and formylation, reduced cytosine hydroxymethylation, decreased histone acetylation, and altered expression levels of multiple genes. Our results suggest that inflammatory processes are responsible for epigenetic changes contributing to lung cancer development.

Acute Respiratory Barrier Disruption by Ozone Exposure in Mice.

Ozone exposure causes irritation, airway hyperreactivity (AHR), inflammation of the airways, and destruction of alveoli (emphysema), the gas exchange area of the lung in human and mice. This review focuses on the acute disruption of the respiratory epithelial barrier in mice. A single high dose ozone exposure (1 ppm for 1 h) causes first a break of the bronchiolar epithelium within 2 h with leak of serum proteins in the broncho-alveolar space, disruption of epithelial tight junctions and cell death, which is followed at 6 h by ROS activation, AHR, myeloid cell recruitment, and remodeling. High ROS levels activate a novel PGAM5 phosphatase dependent cell-death pathway, called oxeiptosis. Bronchiolar cell wall damage and inflammation upon a single ozone exposure are reversible. However, chronic ozone exposure leads to progressive and irreversible loss of alveolar epithelial cells and alveoli with reduced gas exchange space known as emphysema. It is further associated with chronic inflammation and fibrosis of the lung, resembling other environmental pollutants and cigarette smoke in pathogenesis of asthma, and chronic obstructive pulmonary disease (COPD). Here, we review recent data on the mechanisms of ozone induced injury on the different cell types and pathways with a focus on the role of the IL-1 family cytokines and the related IL-33. The relation of chronic ozone exposure induced lung disease with asthma and COPD and the fact that ozone exacerbates asthma and COPD is emphasized.

Environmental stress impairs photoreceptor outer segment (POS) phagocytosis and degradation and induces autofluorescent material accumulation in hiPSC-RPE cells

Retinal pigment epithelium (RPE) cell dysfunction is central to the pathogenesis of age-related macular degeneration (AMD), a leading cause of adult blindness. Aging, the single biggest risk factor for AMD development, favors increase in RPE autofluorescent material due to accumulation of POS-digestion by-products through lysosomal dysfunction and impaired POS degradation. Apart from aging, environmental agents affect lysosomal function in multiple model systems and are implicated in AMD. Iron (Fe) overload and cigarette smoke exposure are the two environmental factors that are known to affect the lysosomal pathway and impact RPE cell health. However, the impact of Fe and cigarette smoke, on POS processing and its consequence for autofluorescent material accumulation in human RPE cells are yet to be established. Human induced pluripotent stem cell (hiPSC)-derived RPE, which phagocytoses and degrades POS in culture and can be derived from control individuals (no history/susceptibility for retinal disease), provides a model system to investigate the singular effect of excess Fe and/or cigarette smoke on POS processing by RPE cells. Using at least three distinct control hiPSC lines, we show that, compared to untreated hiPSC-RPE cells, POS uptake is reduced in both Fe (ferric ammonium citrate or FAC) and FAC + CSE (cigarette smoke extract)-treated hiPSC-RPE cells. Furthermore, exposure of hiPSC-RPE cultures to FAC + CSE leads to reduced levels of active cathepsin-D (CTSD), a lysosomal enzyme involved in POS processing, and causes delayed degradation of POS. Notably, delayed degradation of POS over time (2 weeks) in hiPSC-RPE cells exposed to Fe and CSE was sufficient to increase autofluorescent material build-up in these cells. Given that inefficient POS processing-mediated autofluorescent material accumulation in RPE cells has already been linked to AMD development, our results implicate a causative role of environmental agents, like Fe and cigarette smoke, in AMD.

Cadmium level in brain correlates with memory impairment in F1 and F2 generation mice: improvement with quercetin.

The increased exposure to cadmium (Cd) through environmental pollutants, food and cigarette smoke is a concern worldwide. The association of Cd with impaired learning disabilities led us to hypothesise that cadmium levels in brain tissue could be dose-dependently related to the extent of memory impairment and oxidative stress. In this study, we proposed to study whether cadmium exposure to dams could alter the brain Cd levels, memory parameters, antioxidant enzymes in brain and their gene expression in the F1-F2 generation mice and whether quercetin could modulate this effect. Animals were administered Cd alone and in combination with quercetin for 7days during their gestation period. Their newborn pups (F1 and F2 mice) were reared until adulthood and were tested for memory using Morris water maze and step-down latency test. The brain tissue of F1 mice was collected. Cd levels were estimated using the atomic absorption spectrophotometer. G-S-transferase (GST) and catalase (CAT) activity were measured and fold increase in their respective gene expression was observed using the RT-PCR method. Cd levels were significantly increased in the brain tissue of animals exposed to Cd but cotreatment with quercetin showed decreased levels in both generations. Memory impairment was observed in animals of F1 generation exposed to Cd and cotreatment with quercetin (100mg/kg) reversed this effect. Cd exposure significantly enhanced both activity and expression of GST and CAT in the brain tissue of F1 generation mice and quercetin attenuated this effect. In F2 generation, results were variable. GST activity and expression increased with Cd and decreased with quercetin cotreatment. However, CAT activity showed no significant change despite a decrease in gene expression. Quercetin cotreatment enhanced activity as well gene expression in F2 generation. Our study insinuates that Cd levels could act as a predictor of memory impairment and altered enzyme activity and gene expression in brain tissue. Quercetin helped to reduce Cd levels in brain tissue of F1 and F2 generation and modulated the antioxidant system of the cell by affecting expression of antioxidant enzymes at the transcription level.

MicroRNAs and their role in environmental chemical carcinogenesis

MicroRNAs (miRNAs) are a class of small, noncoding RNA species that play crucial roles across many biological processes and in the pathogenesis of major diseases, including cancer. Recent studies suggest that the expression of miRNA is altered by certain environmental chemicals, including metals, organic pollutants, cigarette smoke, pesticides and carcinogenic drugs. In addition, extensive studies have indicated the existence and importance of miRNA in different cancers, suggesting that cancer-related miRNAs could serve as potential markers for chemically induced cancers. The altered expression of miRNA was considered to be a vital pathogenic role in xenobiotic-induced cancer development. However, the significance of miRNA in the etiology of cancer and the exact mechanisms by which environmental factors alter miRNA expression remain relatively unexplored. Hence, understanding the interaction of miRNAs with environmental chemicals will provide important information on mechanisms underlying the pathogenesis of chemically induced cancers, and effectively diagnose and treat human cancers resulting from chronic or acute carcinogen exposure. This study presents the current evidence that the miRNA deregulation induced by various chemical carcinogens, different cancers caused by environmental carcinogens and the potentially related genes in the onset or progression of cancer. For each carcinogen, the specifically expressed miRNA may be considered as the early biomarkers of the cancer process. In this review, we also summarize various target genes of the altered miRNA, oncogenes or anti-oncogenes, and the existing evidence regarding the gene regulation mechanisms of cancer caused by environmentally induced miRNA alteration. The future perspective of miRNA may become attractive targets for the diagnosis and treatment of carcinogen-induced cancer.

Aspirin abrogates impairment of mammary gland differentiation induced by early in life second-hand smoke in mice.

Epidemiological studies show that there is limited evidence that tobacco smoking causes breast cancer in humans. In rodents, many tobacco smoke chemicals cause mammary gland tumors. This study evaluated the mammary gland differentiation in mice exposed to environmental cigarette smoke (ECS), using 3R4F Kentucky reference cigarettes, starting after birth and continuing daily for 10 weeks (total particulate exposure 95 mg/m3; CO 610 ppm). We also analyzed the effects of oral administration of non-steroidal anti-inflammatory drugs (NSAIDs), aspirin (1600 mg/kg) or naproxen (320 mg/kg), on mammary gland differentiation, either in unexposed or ECS-exposed mice. The ECS exposure caused delay of mammary glands development. We speculate that this delay may result from aryl hydrocarbon receptor (AHR) signaling activation, which has an antiestrogenic effect and crosstalk to the estrogen metabolism pathway. Similarly, naproxen impaired gland differentiation in unexposed and ECS-exposed mice, while aspirin hindered its development only in unexposed mice. The lack of differentiation induced by the NSAIDs could be explained by their antiestrogenic effect through inhibition of aldo-keto reductases. In ECS-exposed animals, aspirin induced intense lobular formation, which could indicate that aspirin is counteracting the AHR signaling induced by ECS. Based on the differentiation induced by aspirin in ECS-exposed animals, we postulate that these mice would be less susceptible to mammary carcinogenesis. Our results suggest that exposure to smoke at an early age impairs the development of the mammary gland, thus resulting in a longer period of susceptibility and increased risk of breast cancer. However, addition of aspirin can abrogate this effect.

The potential of mangrove Avicennia marina and A. Alba from Nguling district, Pasuruan, East Java as an antioxidant

Free radicals are highly reactive molecules due to unpaired electron in their outer orbital. Excess of free radicals inside human body as consequences of environmental exposure such cigarette smoke may lead to degenerative diseases such as diabetic, cancer etc. This negative effect can be limited by the utilization of natural antioxidant substances, especially produced from plant. Avicennia alba dan A. marina are mangrove species that widely distributed in Indonesia and are expected potential as antioxidant. The objective of this study is to evaluated Avicennia alba dan A. marina potency as antioxidant performed with DPPD (1,1-diphenyl-β-picryl hydrazyl) method. Leaf and bark of Avicennia alba dan A. marina were collected from Nguling District, Pasuruan, East Java. Results shows that based on 50% inhibition Concentration (IC50), Avicennia alba leaf were categorized had a very high antioxidant potential (IC50 14,85 ppm) whereas the bark were categorized had a weak antioxidant potential IC50 167,17 ppm). For A. marina, the leaf were categorized had a moderate antioxidant (IC50 123,23 ppm) whereas the bark were categorized had a weak antioxidant potential (IC50 198,15 ppm).

Increase of somatic cell mutations in oxidative damage-sensitive drosophila

BackgroundOxidative damage is an important genotoxic source for almost all organisms. To efficiently detect mutations induced by oxidative damage, we previously developed a urate-null Drosophila strain. Using this Drosophila strain, we showed the mutagenic activity of environmental cigarette smoke (ECS) and the herbicide paraquat, which are known to produce reactive oxygen species (ROS). In the present study, we examined the mutagenic activities of carcinogenic mutagens that are considered to cause mutations by adduct formation, alkylation, or crosslinking of cellular DNA in the oxidative damage-sensitive Drosophila to evaluate how the oxidative damage induced by these mutagens is involved in causing mutations. In addition, we evaluated whether these oxidative damage-sensitive flies may be useful for mutation assays.MethodsWe performed the wing-spot test in oxidative damage-sensitive Drosophila (urate-null strains) to examine the mutagenicity of 2-amino-3,8-dimethylimidazo[4,5-f]-quinoxaline (MeIQx), mitomycin C (MMC), 4-nitroquinoline N-oxide (4NQO), N-nitrosodimethyl-amine (NDMA), and N-nitrosodiethylamine (NDEA). We also observed the mutagenicity of X-ray irradiation as a control in which mutations should be mainly caused by oxidative damage.ResultsAs expected, the mutagenic activity of X-ray irradiation was higher in the urate-null Drosophila than in the wild-type Drosophila. The mutagenic activities of the tested compounds were also higher in the urate-null Drosophila than in the wild-type Drosophila. In experiments using another urate-null strain, the mutagenicity of N-nitrosodialkylamines was also higher in the urate-null flies than in the wild-type ones.ConclusionsThe tested compounds in this study were more mutagenic in urate-null Drosophila than in wild-type Drosophila. It was supposed that ROS were generated and that the ROS might be involved in mutagenesis. The present results support the notion that in addition to causing DNA lesions via adduct formation, alkylation, or DNA crosslinking, these mutagens also cause mutations via ROS-induced DNA damage. As such, urate-null Drosophila appear to be useful for detecting the mutagenic activity of various mutagens, especially those that produce reactive oxygen. If the mutation rate increases on a mutation assay using urate-null Drosophila, it might suggest that the mutagen generates ROS, and that the produced ROS is involved in causing mutations.

The Effects of Exposure to Environmental Cigarette Smoke on the Vocal Folds of Rats

This study aimed to investigate histopathologically and immunohistochemically the effects of environmental smoke on the vocal folds. This study examined 20 healthy Wistar albino rats, which were divided into four groups of five rats. Group 1 was exposed to smoke for 45 days and group 2 for 90 days. Groups 3 and 4 were the respective control groups. The rats in groups 1 and 3 were sacrificed on day 45 and those in groups 2 and 4 on day 90. The larynx specimens were stained with hematoxylin and eosin, and the inflammation, hyperplasia, and metaplasia were evaluated. Ki-67 staining was used for the immunohistochemical analysis. There was no significant difference in mononuclear cell infiltration between the experimental and control groups (group 1 vs. group 3 P = 0.20, group 2 and 4 P = 0.41) (Table 3), but there was a significant difference between the two experimental groups (P = 0.007). Mild and moderate hyperplasia was seen in groups 1 and 2, respectively. Environmental exposure to cigarette smoke has destructive effects on the vocal folds of rats.

Does environmental cigarette smoke affect breastfeeding behavior?

BACKGROUND:Exposure of lactating women to environmental cigarette smoke may increase cotinine in breast milk, which in turn may reduce the volume of milk and the duration of breastfeeding.OBJECTIVES:To assess the relationship between exposure to environmental cigarette smoke and breastfeeding behavior.MATERIALS AND METHODS:This prospective cohort study was conducted on 290 mothers in Babol - Iran, who had been breastfeeding for 3–5 days after delivery. The lactating mothers were divided into two groups: those exposed to environmental cigarette smoke, and those free from smoke exposure. The study questionnaire included demographic data, information on environmental cigarette smoke, and breastfeeding behavior. Data was collected through telephone interviews at 2, 4, and 6 months of follow-up. Statistical analysis included descriptive statistics, and test of significance using Chi-square test, t-test, log-rank test, and Cox proportional hazards model.RESULTS:The continuation of breastfeeding for the group of exposed mothers and the unexposed group was (mean ± standard deviation) 5.57 ± 0.098 and 5.58 ± 0.109, respectively in 6 months of follow-up. There was no significant difference between the two groups (P = 0.93). The percentage of exclusive breastfeeding at 6 months in the group exposed to cigarette smoke was 65% compared to 76% of the nonexposed group. However, the difference was not statistically significant (P = 0.149).CONCLUSIONS:In this study, no significant association was observed between the group exposed to environmental cigarette smoke and the nonexposed group in breastfeeding behavior, although the percentage of exclusive breastfeeding at 6 months was less in the group exposed to environmental cigarette smoke. Further exploratory studies are needed.

Allergy symptoms, serum total immunoglobulin E, and risk of head and neck cancer.

Allergy symptoms have been associated with a reduced head and neck cancer (HNC) risk, while elevated blood immunoglobulin E (IgE) levels have been associated with an increased HNC risk. According to the "prophylaxis hypothesis," allergic reaction is the body's way of expelling carcinogens. IgE level may be increased by exposure to environmental carcinogens, including alcohol and cigarette smoke. We hypothesized that individuals with elevated serum IgE without allergy symptoms (i.e., asymptomatic atopic) would have the highest HNC risk. A case-control study of HNC (576 cases and 740 controls) was conducted to evaluate the association between allergy symptoms or serum total IgE and HNC risk and the effect modification of allergy symptoms on the association between serum total IgE and HNC risk. Elevated serum total IgE was associated with a significantly increased HNC risk [odds ratio (OR) 1.71, 95% confidence interval (CI) 1.21-2.42]. Having allergy symptoms was associated with a significantly reduced HNC risk (OR 0.56, 95% CI 0.43-0.73). Compared to subjects with normal serum total IgE and no allergy symptoms, asymptomatic atopic individuals had a significantly increased HNC risk (OR 2.12, 95% CI 1.33-3.35). Our results provided further evidence to support the "prophylaxis hypothesis." Further investigations regarding the immune profiles of asymptomatic atopic individuals may provide additional clues for the biological mechanisms underlying the association between allergy symptoms, IgE, and HNC risk.

Antenatal counseling against passive smoking may improve birth weight for gestational age

The authors determined the impact of antenatal counseling against exposure to environmental cigarette smoke on the prevention of reduced neonatal birth weight according to gestational age.A cross-sectional study was conducted in pregnant women, with 77 passive smokers and 88 non-smokers. During motivational interviews, passive smoking status was monitored and additional follow-up visits were arranged to increase the knowledge regarding perinatal risks of passive smoking, including intrauterine growth restriction and low birth weight. The authors aimed to increase the woman's motivation to avoid second-hand tobacco smoke exposure.The demographic and clinical findings of the study groups were found considerably similar, in this context, and the authors found positive and strong correlations between the gestational age and neonatal birth weight (r = 0.80 and r = 0.76, respectively; p < 0.05).During antenatal care of women, regular counseling against second-hand smoke exposure may prevent negative effect of passive smoking on neonatal birth weight according to gestational age. This promising finding needs to be supported by further studies with larger sample size considering covariates relevant to passive smoking.

Modulation by aspirin and naproxen of nucleotide alterations and tumors in the lung of mice exposed to environmental cigarette smoke since birth.

Chemoprevention provides an important strategy for cancer control in passive smokers. Due to the crucial role played by smoke-related chronic inflammation in lung carcinogenesis, of special interest are extensively used pharmacological agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs). We evaluated the ability of aspirin and naproxen, inhibitors of both cyclooxygenase-1 and cyclooxygenase -2, to modulate environmental cigarette smoke (ECS)-induced lung carcinogenesis in A/J mice of both genders. Based on a subchronic toxicity study in 180 postweaning mice, we used 1600 mg/kg diet aspirin and 320 mg/kg diet naproxen. In the tumor chemoprevention study, using 320 mice, exposure to ECS started soon after birth and administration of NSAIDs started after weaning. At 10 weeks of life, the NSAIDs did not affect the presence of occult blood in feces. As assessed in a subset of 40 mice, bulky DNA adducts and 8-hydroxy-2'-deoxyguanosine levels were considerably increased in ECS-exposed mice and, irrespective of gender, both NSAIDs remarkably inhibited these nucleotide alterations. After exposure for 4 months followed by 5 months in filtered air, ECS induced a significant increase in the yield of surface lung tumors, the 43.7% of which were adenomas and the 56.3% were adenocarcinomas. Oct-4 (octamer-binding transcription factor 4), a marker of cell stemness, was detected in some adenocarcinoma cells. The NAIDs attenuated the yield of lung tumors, but prevention of ECS-induced lung adenomas was statistically significant only in female mice treated with aspirin, which supports a role for estrogens in ECS-related lung carcinogenesis and highlights the antiestrogenic properties of NSAIDs.

Allergic conjunctivitis: a cross-sectional study.

Ocular allergy is a common disease in daily practice. A cross-sectional study was conducted to evaluate clinical aspects of and therapeutic approaches to ocular allergy in Italy. Of the 3685 patients affected by ocular allergy and enrolled by 304 ophthalmologists nationally, 3545 were eligible to be included in the statistical analysis. A questionnaire was administered in office to record demographic data, comorbidities, trigger factors, number of conjunctivitis episodes, and past treatments. Signs and symptoms were graded according to their severity, frequency, and duration. Mean age of enrolled patients was 38±19years. Seasonal allergic conjunctivitis (55% of patients) was equally distributed among the different age groups, while perennial allergic conjunctivitis (18%) increased with age and vernal keratoconjunctivitis (9%) was more frequent under the age of 18. Itching and redness were reported in 90% and 85%, respectively; lid skin involvement was observed in 22% of cases and keratitis in 11%. Pollen sensitivities were indicated as the most frequent triggers; however, exposure to non-specific environmental conditions, pollutants, and cigarette smoke was frequently reported. Only 35% of patients underwent a diagnostic evaluation of specific allergic sensitization, with positive allergy tests found in 82% of this subset. With regard to treatment, topical decongestants were used in 43% of patients, corticosteroids in 41%, antihistamines in 29%, systemic antihistamines in 27%, and mast cell stabilizers in 15%. This survey provided useful epidemiological information regarding the clinical characteristics and treatment options of a large cohort of patients affected by different forms of ocular allergy. An understanding of ocular allergic disease, its incidence, demographics, and treatment paradigms provides important information towards understanding its pharmacoeconomics and burden on the national health system.