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Journal Article•DOI•

Light-at-night, circadian disruption and breast cancer: assessment of existing evidence

Richard G. Stevens1•
University of Connecticut Health Center1
01 Aug 2009-International Journal of Epidemiology (Oxford University Press)-Vol. 38, Iss: 4, pp 963-970
TL;DR: If a consensus eventually emerges that LAN does increase risk, then the mechanisms for the effect are important to elucidate for intervention and mitigation and will provide for the development of lighting technologies at home and at work that minimize circadian disruption, while maintaining visual efficiency and aesthetics.
Abstract: Background Breast cancer incidence is increasing globally for largely unknown reasons. The possibility that a portion of the breast cancer burden might be explained by the introduction and increasing use of electricity to light the night was suggested >20 years ago. Methods The theory is based on nocturnal light-induced disruption of circadian rhythms, notably reduction of melatonin synthesis. It has formed the basis for a series of predictions including that non-day shift work would increase risk, blind women would be at lower risk, long sleep duration would lower risk and community nighttime light level would co-distribute with breast cancer incidence on the population level. Results Accumulation of epidemiological evidence has accelerated in recent years, reflected in an International Agency for Research on Cancer (IARC) classification of shift work as a probable human carcinogen (2A). There is also a strong rodent model in support of the light-at-night (LAN) idea. Conclusion If a consensus eventually emerges that LAN does increase risk, then the mechanisms for the effect are important to elucidate for intervention and mitigation. The basic understanding of phototransduction for the circadian system, and of the molecular genetics of circadian rhythm generation are both advancing rapidly, and will provide for the development of lighting technologies at home and at work that minimize circadian disruption, while maintaining visual efficiency and aesthetics. In the interim, there are strategies now available to reduce the potential for circadian disruption, which include extending the daily dark period, appreciate nocturnal awakening in the dark, using dim red light for nighttime necessities, and unless recommended by a physician, not taking melatonin tablets.

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Illuminating a bird’s world

[...]

de Maaike Jong
01 Jan 2016
TL;DR: Investigating the effects of artificial light at night on several aspects of avian ecology, including effects on physiology, behaviour, life-history traits, and fitness, by studying common songbirds in the Netherlands found correlations were found between light levels and first egg laying dates.
Abstract: Natural night-time darkness has disappeared across large parts of the world as a result of light pollution, the alteration of light levels in the outdoor environment due to artificial light sources. This increase in sky brightness not only obscures our perception of the starry sky; it can also have severe effects on human health as well as detrimental impacts on nature. Many animals are attracted to light at night and thereby suffer direct fitness losses, but more subtle effects can also occur. One such effect is the timing of daily and seasonal activities. As organisms have evolved under a natural light-dark cycle, which is the main driver for circannual and circadian rhythms, these activities can be disturbed by anthropogenic light at night. One species group that is potentially greatly affected by nocturnal illumination is birds, as species in this group have excellent vision and also possess light sensitive tissue in their brain. Artificial light at night can thus affect many aspects of a bird’s life. Timing of dawn and dusk singing, foraging behaviour, and sleep pattern are for example known to be altered by the presence of street lights. Yet, so far, experimental and especially long term field studies investigating the effects of nocturnal illumination on birds are lacking. Amongst the options to reduce the effects of night-time light pollution on ecosystems is the adaption of the light spectrum. The LED lamps that are used more and more in outdoor lighting have large economic advantages, and their colour composition can be custom-designed. This could potentially mitigate the impact of light on flora and fauna by using a specific light colour that has minimal effects on biological processes. However, little is known about the effects of different colours of light on birds. The aim of this thesis was to investigate the effects of artificial light at night on the ecology of birds. More specifically, the effects of different light colours and light intensities are studied, to provide insight into the possibilities of mitigation. The focus was on investigating the effects of artificial light at night on several aspects of avian ecology, including effects on physiology, behaviour, life-history traits, and fitness, by studying common songbirds in the Netherlands. To this end, three different approaches were used. Firstly, avian timing of breeding was related to levels of light pollution, in a correlational study using long-term data from across the Netherlands. Nocturnal light levels were used as a proxy for the level of urbanisation of an area. Data from ten common, nest box breeding bird species, collected by a citizen science network, were used. For great tits (Parus major), blue tits (Cyanistes caeruleus) and pied flycatchers (Ficedula hypoleuca), correlations were found between light levels and first egg laying dates. However, these correlations were not apparent in all years, and were negative in some years and positive in others. A possible reason for this inconsistency is that this study included few data from the highly urbanized areas of the Netherlands. In order to truly quantify the impact of urbanisation on wild birds, data collection needs to be expanded to include such areas. Secondly, in order to study the breeding ecology of cavity-breeding passerines, a large-scale field experiment was set up in which formerly dark, natural habitat was experimentally illuminated with white, green or red LED light, in addition to a dark control treatment. The experimental nature of the set-up allowed the effects of nocturnal illumination to be tested independently of other anthropogenic disturbances that are normally associated with light at night. The effects of light at night on life-history traits and fitness components in two free-living songbird species, the great tit and the pied flycatcher, were measured in two consecutive years. In 2013, but not in 2014, white and green light advanced the first egg laying date of great tits. Pied flycatchers were unaffected by the light at night. In the same two years, the extra-pair behaviour of the great tit was studied. In 2014, the proportion of extra-pair young in broods increased with distance to the red and white lamps. In 2013, light had no effect. The discrepancies between years in both studies were probably linked to the very different climatic conditions in both years. The effects that were shown in these studies are with regard to the behaviour of birds; so far in our experimental study, no fitness consequences of breeding in lighted areas have been observed, in terms of the reproductive success of pairs, the reproductive success of males when extra-pair offspring is included, or of adult survival to the next breeding season. To study whether the behavioural effects found so far at this experimental set-up were due to the direct or the indirect effects of artificial light at night, male great tits were deployed with light loggers to measure their light exposure over a 24 hour period. Males from pairs breeding close to the lamp posts were not exposed to more light than males from pairs nesting further away. This suggests that male great tits avoid exposure to light at night and thus that the effects of artificial light on behaviour found so far might be indirect rather than direct. Finally, the effects of night-time light colour and intensity on the physiology and behaviour of captive birds were studied, in a controlled laboratory environment. In contrast to the field studies, in this set-up birds were exposed to artificial light levels with no possibility of escaping to darker places. Dose-dependent effects of artificial light at night on birds’ daily activity patterns and melatonin levels were demonstrated in great tits. Higher light intensities advanced activity onset and delayed activity offset. Night-time activity increased and melatonin levels (measured at midnight) decreased at higher light intensities. In two other experiments, the effects of light colour and light intensity on the daily activity patterns of blue tits were studied. In all colours, and most of all in red and white light, birds advanced their onset of activity in the morning. The effect of light intensity on activity onset was smaller in green than in white light in the lower range of intensities, but became equal at the highest intensities. These studies show that different light colours have different effects on activity patterns, and that disturbance to daily activity patterns can be partially mitigated by changes in the characteristics of outdoor lighting. Some of the findings presented in this thesis can be directly translated into advice for policy and conservation; others first need further investigation. Furthermore, all are based on studies of a few bird species. Since the effects of light at night of different spectral compositions do vary widely between species groups, the challenge is going to be in coming up with advice on outdoor lighting for areas with many different species, rather than for just one species or species group. This thesis has begun to uncover the effects of artificial light at night on avian ecology; some novel findings on birds in illuminated nights have been presented and recommendations for future research have been made. In recent years, much has been revealed regarding the biological impacts of anthropogenic nocturnal illumination. Yet, there is much still unknown. The experimental field set-up described here forms an excellent and valuable tool to continue to study the effects of ever-increasing night-time light levels on ecosystems.

2 citations

Cites background from "Light-at-night, circadian disruptio..."

  • ...Potential long term health consequences are difficult to demonstrate experimentally in humans, but a positive association between obesity and exposure to light at night in British women was reported (McFadden et al. 2014) and a correlation with breast cancer has been found (Stevens 2009)....

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  • ...2014) and a correlation with breast cancer has been found (Stevens 2009)....

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Proceedings Article•DOI•
Bio-Clock-Aware Office Lighting Control

[...]

Charikleia Papatsimpa1, J. H. Bonarius1, Jean-Paul M. G. Linnartz1•
Eindhoven University of Technology1
04 Aug 2020
TL;DR: A novel optimization algorithm is introduced that finds the best office lighting profile to achieve circadian alignment to the 24-hour cycle, and aims to support employee’s circadian rhythm and ensure that they receive the right light at the right time of the day.
Abstract: In modern society, humans spend over 90% or their time indoors. However, despite the growing scientific understanding of the impact of light on biological mechanisms, benefits of this understanding are not harvested in practical systems. Existing light in the built environment, offices in particular, is designed predominantly to meet visual performance requirements. Increasing attention is being given to the biological effects of light, especially how it could be used to promote occupants’ health and well-being through the circadian functions that regulate sleep, mood, and alertness. While Human Centric Lighting is being offered based on generic insights on population average experiences, in this paper, we suggest a personalized bio-adaptive office lighting system, controlled to emit a lighting recipe tailored to the individual employee. We introduce a novel optimization algorithm that finds the best office lighting profile to achieve circadian alignment to the 24-hour cycle. The system aims to support employee’s circadian rhythm and ensure that they receive the right light at the right time of the day. In particular, we use existing, commonly accepted chronobiologic models to find the most effective light exposure pattern.

2 citations

Cites background from "Light-at-night, circadian disruptio..."

  • ...In fact, circadian disruption has been associated with mood disorders, including depression, and with health risks such as diabetes, obesity, cardiovascular disease, and cancer [5], [6], [7], [8], [9]....

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Journal Article•DOI•
Artificial Light at Night Reduces Anxiety-like Behavior in Female Mice with Exacerbated Mammary Tumor Growth.

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William H. Walker1, Raegan M. Kvadas1, Laura E. May1, Jennifer A. Liu1, Jacob R. Bumgarner1, James C. Walton1, A. Courtney DeVries1, Robert T. Dauchy2, David E. Blask2, Randy J. Nelson1 •
West Virginia University1, Tulane University2
28 Sep 2021-Cancers
TL;DR: In this paper, the influence of artificial light at night (ALAN) on affective behavior in tumor-bearing mice has been investigated and it was shown that exposure to ALAN accelerates mammary tumor growth and predict that ALAN exacerbates negative affective behaviors in tumorbearing mice.
Abstract: Artificial light at night (ALAN) is a pervasive phenomenon. Although initially assumed to be innocuous, recent research has demonstrated its deleterious effects on physiology and behavior. Exposure to ALAN is associated with disruptions to sleep/wake cycles, development of mood disorders, metabolic disorders, and cancer. However, the influence of ALAN on affective behavior in tumor-bearing mice has not been investigated. We hypothesize that exposure to ALAN accelerates mammary tumor growth and predict that ALAN exacerbates negative affective behaviors in tumor-bearing mice. Adult (>8 weeks) female C3H mice received a unilateral orthotropic injection of FM3A mouse mammary carcinoma cells (1.0 × 105 in 100 μL) into the fourth inguinal mammary gland. Nineteen days after tumor inoculation, mice were tested for sucrose preference (anhedonia-like behavior). The following day, mice were subjected to an open field test (anxiety-like behavior), followed by forced swim testing (depressive-like behavior). Regardless of tumor status, mice housed in ALAN increased body mass through the first ten days. Tumor-bearing ALAN-housed mice demonstrated reduced latency to tumor onset (day 5) and increased terminal tumor volume (day 21). Exposure to ALAN reduced sucrose preference independent of tumor status. Additionally, tumor-bearing mice housed in dark nights demonstrated significantly increased anxiety-like behavior that was normalized via housing in ALAN. Together, these data reaffirm the negative effects of ALAN on tumorigenesis and demonstrate the potential anxiolytic effect of ALAN in the presence of mammary tumors.

2 citations

Journal Article•DOI•
Chronotherapy: a noteworthy focal point in the treatment of cancer?

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Perumal Subramanian1, Jaime Jacqueline Jayapalan2, Onn Haji Hashim2•
Annamalai University1, University of Malaya2
20 Mar 2014-Biological Rhythm Research
TL;DR: This review critically evaluates present knowledge on circadian rhythms in relation to cancer and its management and suggests that the accumulating and coercing evidences could be valuable in formulating the rhythm-based therapy as a remarkable focal point in the management of cancer.
Abstract: In mammalian systems including humans, DNA synthesis, cell cycle and mitotic index are circadian in nature. Disrupted circadian clock leads to disturbed cellular rhythms, metabolism and hormonal balance and is noticeably accountable for the uncontrolled cell division ultimately leading to cancer. About a decade ago, there are fewer evidences on the role of biological clock on tumorigenesis. Currently, a relationship between shift work and cancer, distinctively breast cancer in women and prostate cancer in men, distraction of sleep–wake cycles and augmentation of cancer development, oncostatic effects of melatonin (the internal zeitgeber of circadian system), bidirectional relationships of circadian and immune systems, the prospect of clock genes as tumour suppressors, inaccurate temporal management of oxidative stress and genotoxicity have been recounted, making the crucial role of circadian clock in carcinogenesis. This review critically evaluates present knowledge on circadian rhythms in relation to can...

2 citations

Dissertation•
Professions, expositions professionnelles aux solvants et cancer du sein analyse de deux études épidémiologiques sur les cancers du sein chez l'homme et chez la femme

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Sara Villeneuve
29 Sep 2011
TL;DR: Notre avons etudie le role de la profession and des expositions professionnelles aux solvants petroliers and chlores dans deux etudes epidemiologiques sur les facteurs de risque professionnels des cancers du sein chez l'homme et chez la femme.
Abstract: Notre avons etudie le role de la profession et des expositions professionnelles aux solvants petroliers et chlores dans deux etudes epidemiologiques sur les facteurs de risque professionnels des cancers du sein chez l'homme et chez la femme. A l’inverse du cancer du sein feminin (50000 nouveaux cas par an en France), le cancer du sein chez l’homme est un cancer rare (<500 cas par an). Il constitue cependant un modele interessant pour l’etude des expositions professionnelles qui sont generalement plus elevees chez l’homme que chez la femme. Chez les hommes, nos resultats suggerent un risque de cancer augmente chez les mecaniciens de vehicules a moteur et un role cancerogene des solvants tels que le benzene et le trichlorethylene. Chez les femmes, malgre des risques eleves mais non significatifs dans plusieurs professions, aucune association avec les expositions aux solvants n’etait mise en evidence pour les faibles niveaux d’exposition observes.

2 citations

Cites background from "Light-at-night, circadian disruptio..."

  • ...Indice matrice bruts maximum Probabilité maximale non exposés 52 1152 1,0 Référence 1,0 Référence 1,0 Référence [1-10] 6 137 1,0 [0,4-2,5] 0,9 [0,4-2,1] 0,8 [0,3-2,1] [11-20] 10 204 1,3 [0,6-2,5] 1,2 [0,6-2,4] 1,0 [0,5-2,1] [21-30] 31 350 2,1 [1,3-3,3] 2,1 [1,3-3,4] 1,7 [1,0-3,0] ≥ 31 5 58 1,7 [0,6-4,4] 1,6 [0,6-4,3] 1,4 [0,3-6,5] ptendance =0,004 ptendance =0,01 ptendance =0,05 Intensité maximale (ppm) non exposés 52 1152 1,0 Référence 1,0 Référence 1,0 Référence [25-50] 14 332 1,1 [0,6-2,0] 1,1 [0,6-2,0] 0,9 [0,4-1,6] [51-100] 35 371 2,1 [1,4-3,4] 2,1 [1,4-3,4] 1,7 [1,0-2,9] >100 3 46 1,3 [0,4-4,2] 1,3 [0,4-4,2] 1,0 [0,2-5,0] ptendance =0,01 ptendance =0,02 p=0,10 Fréquence maximale non exposés 52 1152 1,0 Référence 1,0 Référence 1,0 Référence [11-20] 23 405 1,4 [0,9-2,4] 1,3 [0,8-2,2] 1,1 [0,7-2,0] [21-30] 26 294 2,0 [1,2-3,3] 1,9 [1,2-3,3] 1,6 [0,9-2,8] ≥ 31 3 50 1,1 [0,3-3,7] 1,1 [0,3-3,7] 0,7 [0,2-2,9] ptendance =0,02 ptendance =0,04 ptendance =0,26 Durée d'exposition (années) non exposés 52 1152 1,0 Référence 1,0 Référence 1,0 Référence ]0-5] 10 191 1,4 [0,7-2,8] 1,3 [0,6-2,7] 1,2 [0,6-2,6] ]5-10] 5 127 0,9 [0,4-2,4] 0,8 [0,3-2,2] 0,8 [0,3-2,1] >10 37 431 1,9 [1,2-3,0] 1,8 [1,2-2,9] 1,6 [0,9-2,6] ptendance=0,01 ptendance=0,01 ptendance=0,02 Exposition cumulée vie entière (ppm....

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  • ...102 Tableau IV.16: Exposition professionnelle au trichloréthylène et risque de cancer du sein chez la femme Cas N=1230 Témoins N=1315 OR [a] IC 95% OR[b] IC 95% OR[c] IC 95% Indices bruts maximum de la matrice Probabilité maximale non exposées 1099 1160 1,0 Référence 1,0 Référence 1,0 Référence [1-10] 59 77 0,8 [0,6-1,1] 0,8 [0,6-1,2] 0,8 [0,6-1,2] [11-20] 45 47 1,0 [0,7-1,5] 1,1 [0,7-1,7] 1,2 [0,7-1,8] ≥ 21 27 31 0,9 [0,6-1,0] 1,1 [0,6-1,8] 1,2 [0,6-2,1] ptendance=0,46 ptendance=0,93 ptendance=0,77 Intensité maximale (ppm) non exposées 1099 1160 1,0 Référence 1,0 Référence 1,0 Référence [5-50] 103 125 0,9 [0,7-1,1] 0,9 [0,7-1,2] 1,0 [0,7-1,3] ≥ 51 28 30 1,0 [0,6-1,7] 1,1 [0,6-1,9] 1,2 [0,7-2,1] ptendance=0,31 ptendance=0,61 ptendance=0,88 Fréquence maximale non exposées 1099 1160 1,0 Référence 1,0 Référence 1,0 Référence [11-20] 65 83 0,8 [0,6-1,2] 0,9 [0,6-1,3] 0,9 [0,7-1,4] [21-30] 63 67 1,0 [0,7-1,4] 1,0 [0,7-1,5] 1,1 [0,7-1,6] ≥ 31 3 5 0,6 [0,1-2,6] 0,6 [0,1-2,9] 0,8 [0,2-3,7] ptendance=0,41 ptendance=0,75 ptendance=0,95 Durée d'exposition (année) non exposées 1099 1160 1,0 Référence 1,0 Référence 1,0 Référence ]0-5] 59 69 0,9 [0,6-1,3] 1,0 [0,7-1,4] 1,0 [0,7-1,5] ]5-10] 20 33 0,6 [0,4-1,1] 0,7 [0,4-1,3] 0,7 [0,4-1,3] >10 52 53 1,0 [0,7-1,5] 1,1 [0,7-1,7] 1,2 [0,8-1,8] ptendance=0,75 ptendance=0,89 ptendance=0,99 Exposition cumulée vie entière (ppm.année) non exposées 1099 1160 1,0 Référence 1,0 Référence 1,0 Référence Icum 1,71 36 51 0,7 [0,5-1,1] 0,8 [0,5-1,2] 0,8 [0,5-1,3] 1,71≥ Icum 6,56 42 51 0,9 [0,6-1,3] 0,9 [0,6-1,4] 1,0 [0,6-1,5] Icum ≥ 6,56 53 53 1,1 [0,7-1,6] 1,2 [0,8-1,7] 1,3 [0,8-2,0] ptendance=0,84 ptendance=0,47 ptendance=0,26 Exposition cumulée vie entière latence 10 ans (ppm.année) non exposées 1099 1160 1,0 Référence 1,0 Référence 1,0 Référence Icum 1,71 36 51 0,8 [0,5-1,1] 0,8 [0,5-1,2] 0,8 [0,5-1,3] 1,71 ≥ Icum 6,56 42 53 0,9 [0,5-1,3] 0,9 [0,6-1,4] 1,0 [0,6-1,5] Icum ≥ 6,56 53 51 1,3 [0,7-1,6] 1,2 [0,8-1,7] 1,3 [0,8-2] ptendance=0,86 ptendance=0,49 ptendance=0,25 Exposition cumulée vie entière latence 20 ans (ppm.année) non exposées 1109 1178 1,0 Référence 1,0 Référence 1,0 Référence Icum 1,71 39 37 1,1 [0,7-1,6] 1,2 [0,7-1,8] 1,2 [0,8-2,0] 1,71 ≥ Icum 6,56 39 54 0,7 [0,5-1,2] 0,9 [0,5-1,4] 0,9 [0,5-1,5] Icum ≥ 6,56 43 46 1,0 [0,6-1,5] 1,0 [0,7-1,6] 1,1 [0,7-1,8] ptendance=0,70 ptendance=0,75 ptendance=0,65 Exposition cumulée vie entière, probabilité d'exposition > 10% non exposées 1099 1160 1,0 Référence 1,0 Référence 1,0 Référence Icum 4,28 23 23 1,0 [0,6-1,8] 1,2 [0,7-2,2,] 1,3 [0,7-2,3] 4,28≥ Icum 16,39 19 27 0,7 [0,4-1,3] 0,8 [0,5-1,6] 0,9 [0,5-1,7] Icum ≥ 16,39 30 27 1,2 [0,7-2,0] 1,3 [0,8-2,2] 1,5 [0,8-2,6] ptendance=0,71 ptendance=0,43 ptendance=0,27 Exposition moyenne annuelle (ppm) nonexposées 1099 1160 1,0 Référence 1,0 Référence 1,0 Référence Icum 0,28 29 51 0,6 [0,4-0,9] 0,6 [0,4-1,0] 0,6 [0,4-1,0] 0,28 ≥ Icum 0,81 58 49 1,2 [0,8-1,8] 1,4 [0,9-2,1] 1,4 [0,9-2,1] Icum ≥ 0,81 44 55 0,8 [0,6-1,3] 0,9 [0,6-1,4] 1,0 [0,6-1,6] ptendance=0,47 ptendance=0,93 ptendance=0,46 [a] ORs ajustés sur l'âge le département....

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  • ...85 Tableau IV.4: Caractéristiques physiques et mode de vie Cas N=1230 Témoins N=1315 OR IC 95% n % n % Taille à 20 ans (cm) ≤ 155 183 14,9 193 14,7 1,0 Référence ]155-160] 349 28,4 389 29,6 1,0 [0,7-1,2] ]160-170] 584 47,5 623 47,4 1,0 [0,8-1,3] >170 104 8,5 92 7,0 1,2 [0,8-1,7] NSP 10 0,8 18 1,4 - - IMC Femmes de moins de 50 ans < 18,5 - Maigreur 28 2,3 15 1,1 1,9 [1,0-3,7] [18,5-25[ - Poids normal 276 22,4 285 21,7 1,0 Référence [25-35[ - Surpoids 57 4,6 95 7,2 0,6 [0,4-0,9] ≥ 35 - Obésité morbide 26 2,1 49 3,7 0,6 [0,3-0,9] NSP 0 0,0 1 0,1 - - Femmes de 50 ans et plus < 18,5 - Maigreur 15 1,2 20 1,5 0,8 [0,4-1,6] [18,5-25[ - Poids normal 438 35,6 437 33,2 1,0 Référence [25-35[ - Surpoids 254 20,7 266 20,2 1,0 [0,8-1,2] ≥ 35 - Obésité morbide 132 10,7 146 11,1 0,9 [0,7-1,2] NSP 4 0,3 1 0,1 - - Fumeur non fumeur 754 61,3 800 60,8 1,0 Référence Actuel 167 13,6 198 15,1 0,9 [0,7-1,1] Ancien 309 25,1 317 24,1 1,0 [0,8-1,2] Paquet.année non fumeur 754 61,3 800 60,8 1,0 Référence ≤ 2 113 9,2 131 10,0 0,9 [0,7-1,2] [3-10] 136 11,1 151 11,5 0,9 [0,7-1,2] [11-20] 109 8,9 118 9,0 1,0 [0,7-1,3] > 20 103 8,4 98 7,5 1,1 [0,8-1,5] NSP 15 1,2 17 1,3 - - Consommation d'alcool (verres/semaine) (vie entière) jamais ou ≤ 3 v/s 959 78,0 991 75,4 1,0 Référence [4-7] v/s 154 12,5 187 14,2 0,8 [0,7-1,1] [8-14] v/s 67 5,4 87 6,6 0,8 [0,6-1,1] >14 v/s 50 4,1 50 3,8 1,0 [0,7-1,5] Activité physique non 387 31,5 365 27,8 1,0 Référence oui 843 68,5 950 72,2 0,8 [0,7-1,0] ORs ajustés sur l'âge et le département IV.1-5....

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  • ...70 Tableau III.11: Exposition professionnelle au benzène et risque de cancer du sein chez l'homme Cas N=104 Témoins N=1901 OR[a] IC 95% OR[b] IC 95% OR[c] IC 95% Indices de la matrice maximum Probabilité max non exposés 79 1668 1,0 Référence 1,0 Référence 1,0 Référence ]0-10] 3 55 1,1 [0,3-3,8] 1,0 [0,3-3,6] 0,9 [0,3-3,3] ]10-50] 11 65 3,5 [1,7-7,0] 3,3 [1,6-6,7] 2,6 [1,2-5,7] ]50-90] 4 61 1,3 [0,4-3,7] 1,2 [0,4-3,6] 1,0 [0,3-2,9] ≥ 90 7 52 2,7 [1,1-6,2] 2,5 [1,1-5,8] 1,9 [0,8-4,8] ptendance=0,01 ptendance=0,01 ptendance=0,23 Intensité max (ppm) non exposés 79 1668 1,0 Référence 1,0 Référence 1,0 Référence [0,1-1[ 7 80 1,8 [0,8-4,2] 1,7 [0,7-3,9] 1,3 [0,5-3,3] [1-5[ 15 133 2,3 [1,3-4,2] 2,2 [1,2-4,0] 1,7 [0,9-3,4] ≥ 5 3 20 2,7 [0,8-9,6] 2,5 [0,7-9,0] 2,1 [0,5-8,1] ptendance=0,01 ptendance=0,02 ptendance=0,13 Fréquence max non exposés 79 1668 1,0 Référence 1,0 Référence 1,0 Référence [0,5-5[ 5 71 1,5 [0,6-3,9] 1,5 [0,6-3,9] 1,2 [0,4-3,4] [5-30[ 16 143 2,2 [1,2-3,9] 2,0 [1,1-3,7] 1,7 [0,8-3,2] ≥ 30 4 19 4,9 [1,5-14,5] 4,3 [1,3-13,5] 2,9 [0,9-9,9] ptendance 0.001 ptendance=0,001 ptendance=0,04 Durée d'exposition (années) non exposés 79 1669 1,0 Référence 1,0 Référence 1,0 Référence ]0-5] 13 114 2,4 [1,3-4,6] 2,2 [1,1-4,1] 1,8 [0,9-3,8] ]5-10] 8 53 3,2 [1,5-7,2] 3,2 [1,4-7,2] 2,6 [1,1-6,3] > 10 4 65 1,1 [0,4-3,1] 1,1 [0,4-3,1] 0,8 [0,3-2,4] ptendance=0,19 ptendance=0,21 ptendance=0,84 Exposition cumulée vie entière (ppm.année) non exposés 79 1668 1,0 Référence 1,0 Référence 1,0 Référence Icum 0,13 4 76 1,1 [0,4-3,2] 1,0 [0,4-2,9] 0,9 [0,3-2,7] 0,13 ≥ Icum 1,25 13 77 3,2 [1,7-6,1] 3,0 [1,5-5,8] 2,4 [1,2-5,1] Icum ≥ 1,25 8 80 2,1 [1,0-4,5] 2,0 [0,9-4,5] 1,5 [0,7-3,7] ptendance=0,05 ptendance=0,06 ptendance=0,38 Exposition cumulée vie entière latence 10 ans (ppm.années) non exposés 79 1670 1,0 Référence 1,0 Référence 1,0 Référence Icum 0,13 4 76 1,1 [0,4-3,2] 1,0 [0,4-2,9] 0,9 [0,3-2,7] 0,13 ≥ Icum 1,25 14 76 3,6 [1,9-6,7] 3,4 [1,8-6,5] 2,7 [1,3-5,6] Icum ≥ 1,25 7 79 1,8 [0,8-4,2] 1,8 [0,8-4,1] 1,4 [0,6-3,3] ptendance=0,10 ptendance=0,12 ptendance=0,59 Exposition cumulée vie entière latence 20 ans (ppm.années) non exposés 81 1691 1,0 Référence 1,0 Référence 1,0 Référence Icum 0,13 4 69 1,1 [0,4-3,2] 1,1 [0,4-3,2] 0,9 [0,3-2,8] 0,13 ≥ Icum 1,25 12 72 3,1 [1,6-6,1] 2,9 [1,5-5,8] 2,3 [1,1-5,0] Icum ≥ 1,25 7 69 2,0 [0,9-4,5] 1,9 [0,8-4,4] 1,4 [0,6-3,4] ptendance=0,08 ptendance=0,11 ptendance=0,51 Exposition cumulée vie entière, probabilité d'exposition >10% (ppm.années) non exposés 79 1668 1,0 Référence 1,0 Référence 1,0 Référence Icum 0,42 11 59 4,0 [2,0-8,1] 3,5 [1,7-7,3] 2,9 [1,3-6,4] 0,42 ≥ Icum 2,23 6 59 1,9 [0,8-4,6] 1,8 [0,7-4,4] 1,3 [0,5-3,4] Icum ≥ 2,23 5 60 1,7 [0,7-4,5] 1,7 [0,7-4,5] 1,2 [1,2-3,4] ptendance=0,26 ptendance=0,27 ptendance=0,91 Exposition moyenne annuelle (ppm) non exposés 79 1669 1,0 Référence 1,0 Référence 1,0 Référence Icum 0,04 5 75 1,4 [0,5-3,5] 1,3 [0,5-3,4] 1,1 [0,4-3,0] 0,04 ≥ Icum 0,22 10 78 2,5 [1,2-5,1] 2,3 [1,1-4,8] 1,9 [0,8-4,2] Icum ≥ 0,22 10 79 2,7 [1,3-5,4] 2,5 [1,2-5,1] 1,9 [0,9-4,3] ptendance=0,01 ptendance=0,01 ptendance=0,10 [a] ORs ajustés sur l'âge, le pays [b] ORs ajustés sur l'âge, le pays, la consommation d'alcool, le niveau d'éducation et l'IMC [c] ORs ajustés sur l'âge, le pays, la consommation d'alcool, le niveau d'éducation, l'IMC, l'exposition cumulée vie entière au TCE (en classes) et l'exposition aux autres solvants pétroliers (ever/never) 71 III.3-4.2....

    [...]

  • ...Somewhat stronger and more convincing associations for breast cancer risk have emerged from investigations of night-shift work, supposedly acting by a similar mechanism of melatonin suppression [Schernhammer et al., 2006; Stevens, 2009]....

    [...]

References
More filters
Journal Article•DOI•
The environment and disease: association or causation?

[...]

Hill Ab1•
University of London1
01 May 1965-Journal of the Royal Society of Medicine
TL;DR: The criteria outlined in "The Environment and Disease: Association or Causation?" help identify the causes of many diseases, including cancers of the reproductive system.
Abstract: In 1965, Austin Bradford Hill published the article "The Environment and Disease: Association or Causation?" in the Proceedings of the Royal Society of Medicine. In the article, Hill describes nine criteria to determine if an environmental factor, especially a condition or hazard in a work environment, causes an illness. The article arose from an inaugural presidential address Hill gave at the 1965 meeting of the Section of Occupational Medicine of the Royal Society of Medicine in London, England. The criteria he established in the article became known as the Bradford Hill criteria and the medical community refers to them when determining whether an environmental condition causes an illness. The criteria outlined in "The Environment and Disease: Association or Causation?" help identify the causes of many diseases, including cancers of the reproductive system.

6,992 citations

Journal Article•
The environment and disease: association or causation?

[...]

Hill Ab
01 Oct 2005-Bulletin of The World Health Organization
TL;DR: This paper contrasts Bradford Hill’s approach with a currently fashionable framework for reasoning about statistical associations – the Common Task Framework – and suggests why following Bradford Hill, 50+ years on, is still extraordinarily reasonable.
Abstract: In 1965, Sir Austin Bradford Hill offered his thoughts on: “What aspects of [an] association should we especially consider before deciding that the most likely interpretation of it is causation?” He proposed nine means for reasoning about the association, which he named as: strength, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment, and analogy. In this paper, we look at what motivated Bradford Hill to propose we focus on these nine features. We contrast Bradford Hill’s approach with a currently fashionable framework for reasoning about statistical associations – the Common Task Framework. And then suggest why following Bradford Hill, 50+ years on, is still extraordinarily reasonable.

5,542 citations

Journal Article•DOI•
Phototransduction by retinal ganglion cells that set the circadian clock.

[...]

David M. Berson1, Felice A. Dunn1, Motoharu Takao1•
Brown University1
08 Feb 2002-Science
TL;DR: It is shown that retinal ganglion cells innervating the SCN are intrinsically photosensitive, and depolarized in response to light even when all synaptic input from rods and cones was blocked.
Abstract: Light synchronizes mammalian circadian rhythms with environmental time by modulating retinal input to the circadian pacemaker-the suprachiasmatic nucleus (SCN) of the hypothalamus. Such photic entrainment requires neither rods nor cones, the only known retinal photoreceptors. Here, we show that retinal ganglion cells innervating the SCN are intrinsically photosensitive. Unlike other ganglion cells, they depolarized in response to light even when all synaptic input from rods and cones was blocked. The sensitivity, spectral tuning, and slow kinetics of this light response matched those of the photic entrainment mechanism, suggesting that these ganglion cells may be the primary photoreceptors for this system.

3,052 citations

Journal Article•DOI•
Light Suppresses Melatonin Secretion in Humans

[...]

Alfred J. Lewy1, Thomas A. Wehr1, Frederick K. Goodwin1, David A. Newsome1, S. P. Markey1 •
National Institutes of Health1
12 Dec 1980-Science
TL;DR: Findings establish that the human response to light is qualitatively similar to that of other mammals.
Abstract: Bright artificial light suppressed nocturnal secretion of melatonin in six normal human subjects. Room light of less intensity, which is sufficient to suppress melatonin secretion in other mammals, failed to do so in humans. In contrast to the results of previous experiments in which ordinary room light was used, these findings establish that the human response to light is qualitatively similar to that of other mammals.

1,776 citations

Journal Article•DOI•
Action Spectrum for Melatonin Regulation in Humans: Evidence for a Novel Circadian Photoreceptor

[...]

George C. Brainard1, John P. Hanifin1, Jeffrey M. Greeson1, Brenda Byrne1, Gena Glickman1, Edward Gerner1, Mark D. Rollag2 •
Thomas Jefferson University1, Uniformed Services University of the Health Sciences2
15 Aug 2001-The Journal of Neuroscience
TL;DR: The results suggest that, in humans, a single photopigment may be primarily responsible for melatonin suppression, and its peak absorbance appears to be distinct from that of rod and cone cellphotopigments for vision.
Abstract: The photopigment in the human eye that transduces light for circadian and neuroendocrine regulation, is unknown. The aim of this study was to establish an action spectrum for light-induced melatonin suppression that could help elucidate the ocular photoreceptor system for regulating the human pineal gland. Subjects (37 females, 35 males, mean age of 24.5 +/- 0.3 years) were healthy and had normal color vision. Full-field, monochromatic light exposures took place between 2:00 and 3:30 A.M. while subjects' pupils were dilated. Blood samples collected before and after light exposures were quantified for melatonin. Each subject was tested with at least seven different irradiances of one wavelength with a minimum of 1 week between each nighttime exposure. Nighttime melatonin suppression tests (n = 627) were completed with wavelengths from 420 to 600 nm. The data were fit to eight univariant, sigmoidal fluence-response curves (R(2) = 0.81-0.95). The action spectrum constructed from these data fit an opsin template (R(2) = 0.91), which identifies 446-477 nm as the most potent wavelength region providing circadian input for regulating melatonin secretion. The results suggest that, in humans, a single photopigment may be primarily responsible for melatonin suppression, and its peak absorbance appears to be distinct from that of rod and cone cell photopigments for vision. The data also suggest that this new photopigment is retinaldehyde based. These findings suggest that there is a novel opsin photopigment in the human eye that mediates circadian photoreception.

1,708 citations

Related Papers (5)
Carcinogenicity of shift-work, painting, and fire-fighting.

[...]

01 Dec 2007-Lancet Oncology
Kurt Straif, Robert Baan, Yann Grosse, Béatrice Secretan, Fatiha El Ghissassi, Véronique Bouvard, Andrea Altieri, Lamia Benbrahim-Tallaa, Vincent Cogliano 
Rotating Night Shifts and Risk of Breast Cancer in Women Participating in the Nurses' Health Study

[...]

17 Oct 2001-Journal of the National Cancer Institute
Eva S. Schernhammer, Francine Laden, Frank E. Speizer, Walter C. Willett, David J. Hunter, Ichiro Kawachi, Graham A. Colditz 
Night Shift Work, Light at Night, and Risk of Breast Cancer

[...]

17 Oct 2001-Journal of the National Cancer Institute
Scott Davis, Dana K. Mirick, Richard G. Stevens
Night work and breast cancer risk: a systematic review and meta-analysis.

[...]

01 Sep 2005-European Journal of Cancer
Sarah P. Megdal, Candyce H. Kroenke, Candyce H. Kroenke, Francine Laden, Francine Laden, Eero Pukkala, Eva S. Schernhammer, Eva S. Schernhammer 
Night-Shift Work and Risk of Colorectal Cancer in the Nurses’ Health Study

[...]

04 Jun 2003-Journal of the National Cancer Institute
Eva S. Schernhammer, Francine Laden, Frank E. Speizer, Walter C. Willett, David J. Hunter, Ichiro Kawachi, Charles S. Fuchs, Graham A. Colditz