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However, as the increased mortality in PM-selected patients may suggest, PM is less able to take into account the ability of patients to participate in and benefit from CM programs [ 6, 16].
And despite the overwhelming scientific evidence directly linking fine soot particles to premature death, Honeycutt testified before Congress in June 2012 that "some studies even suggest PM makes you live longer".
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Healthy people and people with pre-existing coronary artery disease exhibit a reduction in plasma tissue plasminogen activator in the first 24 hours after exposure to PM, suggesting that PM exposure might impair fibrinolysis.
Epidemiological investigation of patients with coronary artery disease (Hampel et al. 2010) and controlled exposure studies of healthy volunteers (Samet et al. 2009) have shown increased QT intervals after exposure to PM, suggesting that PM exposure may increase the risk of atrial and ventricular arrhythmias.
The first results from case studies suggest that PM that stems from emissions generally assumed to be highly toxic (e.g. biomass combustion and fossil fuel combustion) might lead to results that are similar compared with an assessment of PM using established methods.
These results suggest that pM induced caspase-dependent apoptotic cell death.
These results reveal a novel mechanism for regulating TRPM8 channel activity, and suggest that PM dynamics may play an important role in controlling electrical activity in cold-sensitive neurons.
Accumulated data suggest that PM exposure may lead to pulmonary inflammation (Gong et al. 2003; Li et al. 1996; Salvi et al. 1999).
Studies also suggest that PM and other ambient pollutants may invoke a chronic inflammatory process in the respiratory tract resulting in systemic release of inflammatory and oxidative stress mediators (Campbell 2004).
Investigations conducted in Hamilton Harbor, Ontario, Canada (an industrial area with two steel mills), suggest that PM from air pollution and combustion emissions is the principal factor responsible for eliciting genetic mutations (Somers et al. 2004).
In addition, the present associations of F eNO with outdoor ambient EC and OC but not ambient PM2.5 suggest that PM associations may be missed using total particle mass measurements alone, coherent with our previous findings for ambient EC, OC, and symptoms in asthmatic children in Los Angeles (Delfino et al. 2003).
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