Babies born in the most polluted areas of Britain are up to 50 percent more likely to die, according to new research.
A study of almost eight million infants found dramatic increases in mortality rates among those living near busy roads and factories.
And this applied to all three types of toxic fumes that were analysed – both separately and together.
Known as particulate matter (PM10), nitrogen dioxide (NO2) and sulphur dioxide (SO2), the fine particles are emitted into the atmosphere by transport and industry.
Once breathed into the lungs they can cause respiratory illnesses, and a host of other life threatening diseases.
Dr Sarah Kotecha, of the Cardiff University School of Medicine, said: “We found NO2, PM10 and SO2 are each linked in varying degrees to infant deaths from any cause, and to neonatal and post-neonatal deaths.
“This is an important finding as the pollutants are produced and derived from different sources.”
High levels increased the risk of death during the first year of life by 20 to 50 percent, compared to babies born in the least polluted areas.
What is more, those living near coal fired powered stations that pour out SO2 were 21 percent more likely to die within 28 days – known as a ‘neonatal death’.
Dr Kotecha said: “A possible mechanism to explain this could be the transfer of SO2 via the mother’s placenta to the developing foetus.”
Neonatal deaths and deaths from any cause up to the age of one both rose by between 20 and 40 percent in the most polluted areas.
Post neonatal deaths – between four weeks and a year after birth – went up 30 to 50 percent.
The link between air pollution and child mortality has been known for years. But this is the first study to shed light on the connection between particular chemicals and deaths in babies up to a year old.
The most common source of PM10s is traffic. They can be carried deep into the lungs, causing inflammation. Evidence is growing they reach the developing foetus by travelling through the placenta.
NO2 comes from road transport and electricity generation. It is linked to a higher incidence of acute respiratory infection in children.
It is the first study to shed light on which air pollutants are linked to deaths from any cause in babies up to a year old.
Added Dr Kotecha: “Our findings show although progress has been made, the challenge remains to reduce air pollution in order to reduce the numbers of infant deaths.
“In the meantime, by understanding how pollution affects babies, either directly or via the mother, we may be able to target appropriate therapies or other interventions, depending on the amount of exposure to the different types of pollutants.”
Her team analysed data from 7,984,366 live births and deaths that occurred in England and Wales between 2001 and 2012 obtained from the UK’s Office for National Statistics.
They divided the country into approximately 35,000 small areas, each with a similar population size of 1,500 residents or 650 households.
They obtained pollution data from each area for each year, and calculated the annual pollution exposure before linking it to local death rates.
Information on the average annual pollution in England and Wales between 2001 and 2012 came from the UK’s Department for Environment, Food and Rural Affairs.
A second British study presented at the same conference found children exposed to traffic pollution in the womb and during early life had worse lung function.
Professor Anna Hansell, an environmental epidemiologist at the University of Leicester, said: “We found exposure to road traffic PM10 in very early life showed harmful associations with lung function in eight year olds.
“Associations were stronger among boys, children whose mother had a lower education level or smoked during pregnancy.
“Our findings suggest air pollution in pregnancy and early life has important impacts on lung function in early childhood; it may affect children’s development and potentially also their long term health trajectory.”
They were based on the UK Avon Longitudinal Study of Parents and Children (ALSPAC) – the largest to investigate the impact of PM10s from different sources, including road traffic, on lung development and growth.
Between 1990 and 2008, researchers calculated exposures to PM10 in 13,963 children for each trimester, and at the ages of 0-6 months, 7-12 months and then annually to the age of 15 years.
They measured the volume of air that the children could force out in one second (FEV1) and the maximum amount of air they could forcibly exhale after taking the deepest possible breath (FVC) at the age of eight and 15 years.
The results were adjusted for age, gender and height.
The average amount of PM10 derived from road traffic that the children were exposed to was one microgram per cubic metre of air (mcg/m3), but exposure varied from zero to eight mcg/m3 over the periods measured.
Every 1 mcg/m3 increase above zero in exposure to PM10 from traffic during the first trimester was associated with a 0.8% reduction in lung function
This corresponds to an average reduction in FEV1 and FVC lung function of 14 and 16 millilitres, respectively, by the age of eight years.
The researchers found similar associations for exposure to traffic PM10 during the second and third trimesters, over the whole pregnancy, and up to the age of eight.
Exposure to PM10 from all sources during the third trimester was significantly associated with reduced lung function.
The researchers did not see similar associations between traffic pollution and lung function in children at the age of 15 years.
Prof Hansell said: “We think this may be because air pollution levels, particularly diesel emissions, were reducing over the time that the lung function was increasing in these analyses.
“However, it is also possible that the effect of air pollution is small and that lung growth is able to outpace the adverse effects by teenage years.”
It was unclear how traffic pollution could affect childhood lung function, particularly during pregnancy.
One mechanism could be that particles cross the placenta and disturb the development of the growing foetus’s lungs through oxidative stress – an imbalance between free radical molecules and antioxidants.
Another could be that prenatal exposure could induce epigenetic changes – the altering of the function of genes through environmental factors.
Added Prof Hansell: “It is really important to prioritise reduction of air pollution levels to improve respiratory health.
“In separate work, we have also shown associations with lower lung function in adulthood, suggesting that air pollution contributes to ageing of the lungs.
“Lung health is a marker of general health and associated with numerous other chronic diseases.”
Prof Jorgen Vestbo, of the University of Manchester, chair of the European Respiratory Society’s Advocacy Council who was not involved in the study, said: “Air pollution affects 100 per cent of the population as it cannot be avoided, and these studies highlight the harmful effects that are linked to being exposed to dirty air from the very beginning of our lives.
“Lots of previous research has shown that in the long term, outdoor air pollution can reduce life expectancy, affect lung development, increase asthma incidence and lead to other chronic respiratory diseases.
“Breathing is the most basic human function required to sustain life. We cannot give up the fight for the right to breathe clean air, and we must continue to apply pressure on policymakers to ensure that maximum pollutant levels indicated by the World Health Organisation are not breached across our cities and towns in order to protect the health of young babies, as well as the wider population.”
In 2016, 600,000 children died from acute lower respiratory infections caused by polluted air, according to the World Health Organisation.
Pregnant women exposed to polluted air are more likely to give birth prematurely, and have small, low birth-weight children, it says.
Air pollution also impacts neurodevelopment and cognitive ability and can trigger asthma, and childhood cancer.
Children who have been exposed to high levels of air pollution may be at greater risk for chronic diseases such as cardiovascular disease later in life.