Abstract

Artificial light at night (ALAN) is an increasing anthropogenic pollutant, closely associated with human population density, and now well recognized in both terrestrial and aquatic environments. However, we have a relatively poor understanding of the effects of ALAN in the marine realm. Here, we carried out a field experiment in the coral reef lagoon of Moorea, French Polynesia, to investigate the effects of long-term exposure (18–23 months) to chronic light pollution at night on the survival and growth of wild juvenile orange-fin anemonefish, Amphiprion chrysopterus. Long-term exposure to environmentally relevant underwater illuminance (mean: 4.3 lux), reduced survival (mean: 36%) and growth (mean: 44%) of juvenile anemonefish compared to that of juveniles exposed to natural moonlight underwater (mean: 0.03 lux). Our study carried out in an ecologically realistic situation in which the direct effects of artificial lighting on juvenile anemonefish are combined with the indirect consequences of artificial lighting on other species, such as their competitors, predators, and prey, revealed the negative impacts of ALAN on life-history traits. Not only are there immediate impacts of ALAN on mortality, but the decreased growth of surviving individuals may also have considerable fitness consequences later in life. Future studies examining the mechanisms behind these findings are vital to understand how organisms can cope and survive in nature under this globally increasing pollutant.

Extract

In conclusion, combining the growing number of studies showing the negative impacts of ALAN in marine ecosystems with the projections of global population increases, especially along coastlines and the close association with levels of light pollution and population density, ALAN is already a risk to our marine ecosystems and will only exacerbate in the future. Marine-protected areas (MPAs) are not excluded from ALAN and due to the current lack of legislation, 20% of MPAs are already exposed to ALAN and 14.7% are exposed to increasing levels of light pollution [79], therefore mitigation measures should be of paramount importance. Mitigation measures and policy changes are urgently needed including maintaining and creating dark areas, only lighting part of the night and improving lighting technology in terms of directing light where it is needed, reducing light intensities, and changing spectra [80]. There is also growing concern regarding the combined interactions of multiple anthropogenic stressors, such as light and sound pollution [29,30] and the worldwide impact of these cumulative stressors needs to be better understood to help future management strategies [81].

https://royalsocietypublishing.org/doi/10.1098/rspb.2021.0454

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Abstract

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 upstream 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.

https://pubmed.ncbi.nlm.nih.gov/33838441/

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Credit for this post: Dr Pri Bandara Consultant/educator/speaker – Environmental Health https://www.linkedin.com/pulse/how-many-doctors-get-training-non-ionizing-radiation-related-bandara/

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