Posted by Harry Cockburn | 5 months ago
A major study into levels of fine particulate matter (PM2.5) in cities around the world has found significant regional changes in the average level of the dangerous pollutants in the air over the past two decades, and revealed the problem caused around 1.8 million excess deaths in 2019 alone.
The study examined PM2.5 concentrations and associated mortality trends in over 13,000 cities between 2000-2019 and found average PM2.5 concentrations were seven times higher than the World Health Organisation's limits.
Delhi disappears into the smog. India is among the countries worst affected by air pollution
The authors of the study estimated that 61 in every 100,000 deaths in urban areas was attributable to PM2.5 in 2019.
The study found considerable variations by region, with significant falls in air pollution in parts of Africa (18 per cent), Europe (21 per cent) and North and South America (29 per cent). Meanwhile urban areas in Southeast Asia, including India, saw the largest regional increases, with a 27 per cent increase in average population-weighted PM2.5 concentration between 2000-2019.
Southeast Asian cities also saw the largest increase in PM2.5-attributable mortality rates over this period, increasing by 33 per cent from 63 to 84 in 100,000 people.
But despite these disparities, the authors said the decreasing air pollution levels in some areas did not correspond to the same level of decreases in PM2.5-attributable mortality rates on their own.
They said this demonstrates that “other demographic factors, for example, an ageing population and poor general health, are influential drivers of pollution-related mortality burdens”.
Veronica Southerland of George Washington University, and lead author of the study, said: “The majority of the world’s urban population still live in areas with unhealthy levels of PM2.5.
“Avoiding the large public health burden caused by air pollution will require strategies that not only reduce emissions but also improve overall public health to reduce vulnerability.”
In a second study by the same team which looked at the impact of nitrogen dioxide – closely associated with vehicle emissions in urban areas, the scientists found nearly 2 million new cases of paediatric asthma every year could be caused by a traffic-related air pollution.
Also using the data from the same 13,000 cities as the first study, the second piece of research revealed the huge health burden of breathing poisonous air.
“Our study found that nitrogen dioxide puts children at risk of developing asthma and the problem is especially acute in urban areas,” said Susan Anenberg, a co-lead author of the article and a professor of environmental and occupational health at the George Washington University.
“The findings suggest that clean air must be a critical part of strategies aimed at keeping children healthy.”
The study found that out of an estimated 1.85 million new paediatric asthma cases attributed to NO2 globally in 2019, two-thirds occurred in urban areas.
Again there were significant differences found between different parts of the globe, with south Asia and sub-Saharan Africa worst affected.
But overall paediatric asthma cases linked to NO2 fell from 20 per cent of all asthma cases in 2000 to 16 per cent in 2019.
The research team said this “good news means that cleaner air in Europe and parts of the US [has] resulted in big health benefits for children, especially those living in neighbourhoods near busy roadways and industrial sites”.
But they warned that “much more needs to be done, both in higher income countries and in parts of the world still struggling to curb harmful emissions from vehicles and other sources of NO2”.
Dr Anenberg said: “Reducing fossil fuel-powered transportation can help children and adults breathe easier and may pay big health dividends, such as fewer cases of paediatric asthma and excess deaths.
“At the same time, it would also reduce greenhouse gas emissions, leading to a healthier climate.”
Both studies are published in the journal Lancet Planetary Health.