Air pollution has become the disease for every part of the country & this affects quite good human being in the nature of their health care . To add fuel to the fire the living condition & habits of the people create the problem of their health due to the such air pollution . It is the good environment for health care joining with the all condition of cleanness of Road, Water, Garbage, are playing also an indirect part of the health problem adding the environment of air pollution .
Yes, it is related with the amount of pollution in the air. For instance cardiovascular diseases. I use a methodology from Harvard University that related pollution with this problems, specially those pollutants like NOx, SOx and pm2.5.
For more information you can read the paper below:
The WHO estimated the effects of combustion-related particulate matter on life expectancy. The results of this analysis indicate that current exposure to particulate matter from anthropogenic sources leads to an average loss of 8.6 months of life expectancy in Europe. The impacts vary from around 3 months in Finland to more than 13 months in Belgium.
Along similar lines, cleaner air has contributed to increased life expectancy in the US (Pope et al. N Engl J Med. 2009). A decrease of 10 μg/m3 in the concentration of fine particulate matter was associated with an estimated increase in life expectancy of 7.3 months. Fifteen percent of the overall increase in life expectancy over a two decade period was attributed to reductions in air pollution.
The effect on reduced life expectancy is one of the main drivers to further reduce air pollution. The ERC funded ENVIRONAGE project (ENVIRonmental influence ON AGEing in early life) revealed molecular evidence for this accelerated ageing effects over the life course. Recent studies show that the estimated effects of particulate air pollution exposure on the telomere mitochondrial axis of aging may play an important role in chronic health effects of air pollution. Telomeres are nucleoprotein structures that cap the end of chromosomes. They can consist of up to several thousands of tandem-repeated TTAGGG sequences that interact with proteins from the shelterin complex to maintain genomic stability and protect from DNA repair mechanisms. With each cellular division telomeres shorten. Generally, telomere length has been associated with age-related diseases such as cardiovascular disease, type 2 diabetes, insulin resistance, atherosclerosis, and mortality, and is considered as a marker of biological aging.
It has been shown that every 5 µg/m3 increase in PM-2.5 exposure results in a median reduction in telomere length of 16.1 % (95 % confidence interval of -26.0 to -7.4). This finding is consistent with a statistically significant decrease of two other related ageing biomarkers: blood mitochondrial DNA content (MtDNA copy number) and Sirtuin 1 (SRT1) gene expression (Pieters et al. Environ Helath Perspect 2016). This finding supports the influence of longterm exposure to air pollution on the ‘core axis of ageing’ (Martens et al. Environ Health Reports 2016).
In additon, to the observations in adults we found evidence in a large birth cohort (including more than 600 newborns) that telomeres are shorter in fetuses and newborn babies whose mothers had higher exposure to air pollution during pregnancy. A 5 µg/m³ increment in PM2·5 exposure during the entire pregnancy was associated with 7·2% shorter (95% CI: -12·3 to -1·8%) cord blood leukocyte telomeres and 13·3% shorter (95% CI: -19·3 to -6·9%) placental telomere length. The findings were robust and could not be explained by other factors including socio-economic factors, ethnicity or maternal life-style factors.
The observed telomere loss in newborns by prenatal air pollution exposure indicates less buffer for postnatal influences of factors decreasing telomere length and this may increase the risk for chronic diseases in adulthood. This study adds to the growing body of knowledge that exposure to air pollution is related to the ageing phenotype, and that this observation even may have its origins during the in utero life. (Martens et al. JAMA Pediatr 2017).