A new coronavirus (SARS-CoV-2) has determined a pneumonia outbreak in China (Wuhan, Hubei Province) in December 2019, called COVID-19 disease. In addition to the person-to person transmission dynamic of the novel respiratory virus, it has been recently studied the role of environmental factors in accelerate SARS-CoV-2 spread and its lethality. The time being, air pollution has been identified as the largest environmental cause of disease and premature death in the world. It affects body's immunity, making people more vulnerable to pathogens. The hypothesis that air pollution, resulting from a combination of factors such as meteorological data, level of industrialization as well as regional topography, can acts both as a carrier of the infection and as a worsening factor of the health impact of COVID-19 disease, has been raised recently. With this review, we want to provide an update state of art relating the role of air pollution, in particular PM 2.5 , PM 10 and NO 2 , in COVID-19 spread and lethality. The Authors, who first investigated this association, often used different research methods or not all include confounding factors whenever possible. In addition, to date incidence data are underestimated in all countries and to a lesser extent also mortality data. For this reason, the cases included in the reviewed studies cannot be considered conclusive. Although it determines important limitations for direct comparison of results, and more studies are needed to strengthen scientific evidences and support firm conclusions, major findings are consistent, highlighting the important contribution of PM 2.5 and NO 2 as triggering of the COVID-19 spread and lethality, and with a less extent also PM 10 , although the potential effect of airborne virus exposure it has not been still demonstrated.

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ObjectiveTo evaluate the safety and efficacy as a tool of smoking cessation of electronic cigarettes (e-cigarettes), directly comparing users of e-cigarettes only, smokers of tobacco cigarettes only, and smokers of both.DesignProspective cohort study. Final results are expected in 2019, but given the urgency of data to support policies on electronic smoking, we report the results of the 12-month follow-up.Data SourcesDirect contact and structured questionnaires by phone or via internet.MethodsAdults (30–75 years) were included if they were smokers of ≥1 tobacco cigarette/day (tobacco smokers), users of any type of e-cigarettes, inhaling ≥50 puffs weekly (e-smokers), or smokers of both tobacco and e-cigarettes (dual smokers). Carbon monoxide levels were tested in a sample of those declaring tobacco smoking abstinence.Main Outcome MeasuresSustained smoking abstinence from tobacco smoking at 12 months, reduction in the number of tobacco cigarettes smoked daily.Data SynthesisWe used linear and logistic regression, with region as cluster unit.ResultsFollow-up data were available for 236 e-smokers, 491 tobacco smokers, and 232 dual smokers (overall response rate 70.8%). All e-smokers were tobacco ex-smokers. At 12 months, 61.9% of the e-smokers were still abstinent from tobacco smoking; 20.6% of the tobacco smokers and 22.0% of the dual smokers achieved tobacco abstinence. Adjusting for potential confounders, tobacco smoking abstinence or cessation remained significantly more likely among e-smokers (adjusted OR 5.19; 95% CI: 3.35–8.02), whereas adding e-cigarettes to tobacco smoking did not enhance the likelihood of quitting tobacco and did not reduce tobacco cigarette consumption. E-smokers showed a minimal but significantly higher increase in self-rated health than other smokers. Non significant differences were found in self-reported serious adverse events (eleven overall).ConclusionsAdding e-cigarettes to tobacco smoking did not facilitate smoking cessation or reduction. If e-cigarette safety will be confirmed, however, the use of e-cigarettes alone may facilitate quitters remaining so.Registration NumberNCT01785537.

Environmental factors are recognized as risk factors of thyroid cancer in humans. Exposure to radiation, both from nuclear weapon or fallout or medical radiation, and to some organic and inorganic chemical toxicants represent a worldwide public health issue for their proven carcinogenicity. Halogenated compounds, such as organochlorines and pesticides, are able to disrupt thyroid function. Polychlorinated biphenyls and their metabolites and polybrominated diethyl ethers bind to thyroid, transport proteins, replace thyroxin, and disrupt thyroid function as phthalates and bisphenolates do, highly mimicking thyroid hormones. A better knowledge of environmental risks represents a very important tool for cancer prevention through true risks prevention and management. This approach is very important because of the epigenetic origin’s theory of cancer. Therefore, the aim of this review was study the association between environmental agents and thyroid cancer promotion.

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