Light pollution is fundamentally an often harmful alteration of the natural and normally low levels of light, which would be present in the nocturnal environment, in the absence of artificial lights. This alteration causes damage of a different nature.
Among the environmental damage can be listed, like difficulty or loss of orientation in various animal species (migratory birds, sea turtles, nocturnal moths, bats), alteration of the photoperiod in some plants, alteration of circadian rhythms in plants, in animals (such as man) and in microorganisms, stunted growth of the perifiton.
The study: Effects of dim artificial light at night on locomotor activity, cardiovascular physiology, and circadian clock genes in a diurnal songbird, published on the Environmental pollution, explained: "Artificial light is transforming the nighttime environment and quickly becoming one of the most pervasive pollutants on earth.
Across taxa, light entrains endogenous circadian clocks that function to synchronize behavioral and physiological rhythms with natural photoperiod. Artificial light at night (ALAN) disrupts these photoperiodic cues and has consequences for humans and wildlife including sleep disruption, physiological stress and increased risk of cardiovascular disease.
However, the mechanisms underlying organismal responses to dim ALAN, resembling light pollution, remain elusive. Light pollution exists in the environment at lower levels (<5 lux) than tested in many laboratory studies that link ALAN to circadian rhythm disruption.
Few studies have linked dim ALAN to both the u pstream regulators of circadian rhythms and downstream behavioral and physiological consequences. We exposed zebra finches (Taeniopygia gutatta) to dim ALAN (1.5 lux) and measured circadian expression of five pacemaker genes in central and peripheral tissues, plasma melatonin, locomotor activity, and biomarkers of cardiovascular health.
ALAN caused an increase in nighttime activity and, for males, cardiac hypertrophy. Moreover, downstream effects were detectable after just short duration exposure (10 days) and at dim levels that mimic the intensity of environmental light pollution.
However, ALAN did not affect circulating melatonin nor oscillations of circadian gene expression in the central clock (brain) or liver. These findings suggest that dim ALAN can alter behavior and physiology without strong shifts in the rhythmic expression of molecular circadian pacemakers.
Approaches that focus on ecologically-relevant ALAN and link complex biological pathways are necessary to understand the mechanisms underlying vertebrate responses to light pollution."