What caused the Mesozoic-Cenozoic radiation?

The Phanerozoic eon has had 5 major extinction events and 3 major radiation events. After the Cambrian and Ordovician radiations came all five of the major extinction events, the last of which (Cretaceous-Paleogene) occurred during the last major radiation event (Mesozoic-Cenozoic). This timeline suggests the freeing of previously occupied ecological niches isn't the primary driver of major radiations. (However, the Cretaceous-Palaeogene extinction freed niches during the Mesozoic-Cenozoic radiation, and this may be part of why it continued for so long rather than being a purely Mesozoic event.) Although Wikipedia generally gives a good account of suggested reasons for major extinctions, and also for the Cambrian and Ordovician radiation events, it provides no real such detail for the Mesozoic-Cenozoic radiation. What are its conjectured causes?

There is no real start to a radiation event.

First there are many mass extinctions and many radiation events, what you are referring to are just the most notable ones. also the big five do not occur after the odrivian the first occurs directly before. Radiation events happen after every mass extinction even minor ones, the amount of radiation corresponds well with the severity of the extinction. The big five and the big three are just the ones we find the most interesting, not the largest, note graph below). The ordovician radiation event happened directly after the cambrian-ordovician extinction event for instance. And there was a massive diversification after the P_T extinction, it just does not get as much press because almost all the major players become extinct in later extinction events and becasue there are fewer fossils from that time period. Every extinction event is followed by a radiation event. the Mesozoic-Cenozoic radiation is a large radiation because of the KT mass extinction otherwise it would just be the normal background biodiversity turnover.

Essentially radiations are always happening, there is always some radiation going one in some clades. But if you suddenly wipe out a large number of species and organisms, many of those what survive will be the ones that were radiating simple becasue they were small fast breeding generalists which is also the group that radiate a lot. Small fast breeding generalists are what what best survive mass extinctions and a group that does a lot of radiating. There is also a large anthropomorphic component to this, if you take the tree of life and make a radom slice across it anywhere it sill look like many of the groups that survive are radiating becasue all the other radiation events are cut off, while we ignore stable groups becasue they are stable. You can even notice that the radiation of different groups start at different times but then explode after the event. Almost as if our artificial lines between groups is not a great predictor of diversification events. Radiation events are not one off occurrences with clear cut beginnings and ends but a prolonged uptick in an ongoing system with a lot of variation. there is no clear cut start to radiation events imagine trying to pick the exact second summer or winter begins using nothing but temperature data, there is just to much noise due to local and daily condition to make any such point anything but arbitrary.

So the large scale radiations is still caused by the extinction event, it however will almost always look like it was happening earlier becasue on a small scale it never really stops, and where we draw the lines for groups does not correlate well with radiation events, yet we still use it to decide which "groups" are radiating.


If you look at this paper and its graph you can see this effect in angiosperms. The group originates and begins to diversify before the KT but a massive upswing in diversity happens after (actually fairly long after, once the climate/extinction has stabilized)

The Causes of Climate Change

Scientists attribute the global warming trend observed since the mid-20 th century to the human expansion of the "greenhouse effect" 1 &mdash warming that results when the atmosphere traps heat radiating from Earth toward space.

Certain gases in the atmosphere block heat from escaping. Long-lived gases that remain semi-permanently in the atmosphere and do not respond physically or chemically to changes in temperature are described as "forcing" climate change. Gases, such as water vapor, which respond physically or chemically to changes in temperature are seen as "feedbacks."

Gases that contribute to the greenhouse effect include:

  • Water vapor. The most abundant greenhouse gas, but importantly, it acts as a feedback to the climate. Water vapor increases as the Earth's atmosphere warms, but so does the possibility of clouds and precipitation, making these some of the most important feedback mechanisms to the greenhouse effect.
  • Carbon dioxide (CO2). A minor but very important component of the atmosphere, carbon dioxide is released through natural processes such as respiration and volcano eruptions and through human activities such as deforestation, land use changes, and burning fossil fuels. Humans have increased atmospheric CO2 concentration by 48% since the Industrial Revolution began. This is the most important long-lived "forcing" of climate change.
  • Methane. A hydrocarbon gas produced both through natural sources and human activities, including the decomposition of wastes in landfills, agriculture, and especially rice cultivation, as well as ruminant digestion and manure management associated with domestic livestock. On a molecule-for-molecule basis, methane is a far more active greenhouse gas than carbon dioxide, but also one which is much less abundant in the atmosphere.
  • Nitrous oxide. A powerful greenhouse gas produced by soil cultivation practices, especially the use of commercial and organic fertilizers, fossil fuel combustion, nitric acid production, and biomass burning.
  • Chlorofluorocarbons (CFCs). Synthetic compounds entirely of industrial origin used in a number of applications, but now largely regulated in production and release to the atmosphere by international agreement for their ability to contribute to destruction of the ozone layer. They are also greenhouse gases.

Not enough greenhouse effect: The planet Mars has a very thin atmosphere, nearly all carbon dioxide. Because of the low atmospheric pressure, and with little to no methane or water vapor to reinforce the weak greenhouse effect, Mars has a largely frozen surface that shows no evidence of life.

Too much greenhouse effect: The atmosphere of Venus, like Mars, is nearly all carbon dioxide. But Venus has about 154,000 times as much carbon dioxide in its atmosphere as Earth (and about 19,000 times as much as Mars does), producing a runaway greenhouse effect and a surface temperature hot enough to melt lead.

On Earth, human activities are changing the natural greenhouse. Over the last century the burning of fossil fuels like coal and oil has increased the concentration of atmospheric carbon dioxide (CO2). This happens because the coal or oil burning process combines carbon with oxygen in the air to make CO2. To a lesser extent, the clearing of land for agriculture, industry, and other human activities has increased concentrations of greenhouse gases.

The consequences of changing the natural atmospheric greenhouse are difficult to predict, but some effects seem likely:

  • On average, Earth will become warmer. Some regions may welcome warmer temperatures, but others may not.
  • Warmer conditions will probably lead to more evaporation and precipitation overall, but individual regions will vary, some becoming wetter and others dryer.
  • A stronger greenhouse effect will warm the ocean and partially melt glaciers and ice sheets, increasing sea level. Ocean water also will expand if it warms, contributing further to sea level rise.

Outside of a greenhouse, higher atmospheric carbon dioxide (CO2) levels can have both positive and negative effects on crop yields. Some laboratory experiments suggest that elevated CO2 levels can increase plant growth. However, other factors, such as changing temperatures, ozone, and water and nutrient constraints, may more than counteract anypotential increase in yield. If optimal temperature ranges for some crops are exceeded, earlier possible gains in yield may be reduced or reversed altogether.

Climate extremes, such as droughts, floods and extreme temperatures, can lead to crop losses and threaten the livelihoods of agricultural producers and the food security of communities worldwide. Depending on the crop and ecosystem, weeds, pests, and fungi can also thrive under warmer temperatures, wetter climates, and increased CO2 levels, and climate change will likely increase weeds and pests.

Finally, although rising CO2 can stimulate plant growth, research has shown that it can also reduce the nutritional value of most food crops by reducing the concentrations of protein and essential minerals in most plant species. Climate change can cause new patterns of pests and diseases to emerge, affecting plants, animals and humans, and posing new risks for food security, food safety and human health. 2

The Role of Human Activity

In its Fifth Assessment Report, the Intergovernmental Panel on Climate Change, a group of 1,300 independent scientific experts from countries all over the world under the auspices of the United Nations, concluded there's a more than 95 percent probability that human activities over the past 50 years have warmed our planet.

The industrial activities that our modern civilization depends upon have raised atmospheric carbon dioxide levels from 280 parts per million to 416 parts per million in the last 150 years. The panel also concluded there's a better than 95 percent probability that human-produced greenhouse gases such as carbon dioxide, methane and nitrous oxide have caused much of the observed increase in Earth's temperatures over the past 50 years.

Solar Irradiance

The above graph compares global surface temperature changes (red line) and the Sun's energy that Earth receives (yellow line) in watts (units of energy) per square meter since 1880. The lighter/thinner lines show the yearly levels while the heavier/thicker lines show the 11-year average trends. Eleven-year averages are used to reduce the year-to-year natural noise in the data, making the underlying trends more obvious.

The amount of solar energy that Earth receives has followed the Sun&rsquos natural 11-year cycle of small ups and downs with no net increase since the 1950s. Over the same period, global temperature has risen markedly. It is therefore extremely unlikely that the Sun has caused the observed global temperature warming trend over the past half-century. Credit: NASA/JPL-Caltech

It's reasonable to assume that changes in the Sun's energy output would cause the climate to change, since the Sun is the fundamental source of energy that drives our climate system.

Indeed, studies show that solar variability has played a role in past climate changes. For example, a decrease in solar activity coupled with an increase in volcanic activity is thought to have helped trigger the Little Ice Age between approximately 1650 and 1850, when Greenland cooled from 1410 to the 1720s and glaciers advanced in the Alps.

But several lines of evidence show that current global warming cannot be explained by changes in energy from the Sun:

  • Since 1750, the average amount of energy coming from the Sun either remained constant or increased slightly.
  • If the warming were caused by a more active Sun, then scientists would expect to see warmer temperatures in all layers of the atmosphere. Instead, they have observed a cooling in the upper atmosphere, and a warming at the surface and in the lower parts of the atmosphere. That's because greenhouse gases are trapping heat in the lower atmosphere.
  • Climate models that include solar irradiance changes can&rsquot reproduce the observed temperature trend over the past century or more without including a rise in greenhouse gases.


Mike Lockwood, &ldquoSolar Change and Climate: an update in the light of the current exceptional solar minimum,&rdquo Proceedings of the Royal Society A, 2 December 2009, doi 10.1098/rspa.2009.0519

Judith Lean, &ldquoCycles and trends in solar irradiance and climate,&rdquo Wiley Interdisciplinary Reviews: Climate Change, vol. 1, January/February 2010, 111-122.

Acute Radiation Syndrome from Large Exposures

A very high level of radiation exposure delivered over a short period of time can cause symptoms such as nausea and vomiting within hours and can sometimes result in death over the following days or weeks. This is known as acute radiation syndrome, commonly known as “radiation sickness.”

It takes a very high radiation exposure to cause acute radiation syndrome—more than 0.75 gray grayA gray is the international unit used to measure absorbed dose (the amount of radiation absorbed by an object or person). The U.S. unit for absorbed dose is the rad. One gray is equal to 100 rads. (75 rad) radThe U.S. unit used to measure absorbed radiation dose (the amount of radiation absorbed by an object or person). The international equivalent is the Gray (Gy). One hundred rads are equal to 1 Gray. in a short time span (minutes to hours). This level of radiation would be like getting the radiation from 18,000 chest x-rays distributed over your entire body in this short period. Acute radiation syndrome is rare, and comes from extreme events like a nuclear explosion or accidental handling or rupture of a highly radioactive source.

Microwave radiation induced oxidative stress, cognitive impairment and inflammation in brain of Fischer rats

Public concerns over possible adverse effects of microwave radiation emitted by mobile phones on health are increasing. To evaluate the intensity of oxidative stress, cognitive impairment and inflammation in brain of Fischer rats exposed to microwave radiation, male Fischer-344 rats were exposed to 900 MHz microwave radiation (SAR = 5.953 x 10(-4) W/kg) and 1800 MHz microwave radiation (SAR = 5.835 x 10(-4) W/kg) for 30 days (2 h/day). Significant impairment in cognitive function and induction of oxidative stress in brain tissues of microwave exposed rats were observed in comparison with sham exposed groups. Further, significant increase in level of cytokines (IL-6 and TNF-alpha) was also observed following microwave exposure. Results of the present study indicated that increased oxidative stress due to microwave exposure may contribute to cognitive impairment and inflammation in brain.

Cutaneous Radiation Syndrome (CRS)

The concept of cutaneous radiation syndrome (CRS) was introduced in recent years to describe the complex pathological syndrome that results from acute radiation exposure to the skin.

ARS usually will be accompanied by some skin damage. It is also possible to receive a damaging dose to the skin without symptoms of ARS, especially with acute exposures to beta radiation or X-rays. Sometimes this occurs when radioactive materials contaminate a patient&rsquos skin or clothes.

When the basal cell layer of the skin is damaged by radiation, inflammation, erythema, and dry or moist desquamation can occur. Also, hair follicles may be damaged, causing epilation. Within a few hours after irradiation, a transient and inconsistent erythema (associated with itching) can occur. Then, a latent phase may occur and last from a few days up to several weeks, when intense reddening, blistering, and ulceration of the irradiated site are visible.

In most cases, healing occurs by regenerative means however, very large skin doses can cause permanent hair loss, damaged sebaceous and sweat glands, atrophy, fibrosis, decreased or increased skin pigmentation, and ulceration or necrosis of the exposed tissue.


Patient factors and individual variations

Individual patient phenotypic factors have been suggested to influence the susceptibility to intestinal radiation injury. It was reported that older patient age is associated with an increased risk of developing reduced organ function after radiotherapy[102-104]. Body habitus has been reported as another susceptibility factor, where thin patients with narrow antero-posterior diameter can suffer an increased risk of intestinal radiation toxicity compared to normal individuals[36]. Smoking status has been associated with risk of chronic intestinal toxicity[20,105] as well as previous history of surgery[13,35,36].

Medical co-morbidities

Vascular disease: Co-morbid vascular disease such as hypertension, diabetes mellitus and atherosclerosis were suggested to predispose patients to an increased vascular injury following radiation and subsequent intestinal wall ischemia and impaired tissue repair[74]. The microocclusive vascular disease in addition to increased blood viscosity in diabetes mellitus were suggested to predispose to intestinal tissue ischemia[106,107]. One study investigated the possible effect of diabetes mellitus during prostate cancer radiotherapy. The study reported higher rates of late genitourinary/gastrointestinal toxicities in diabetic patients than in non-diabetics (34% and 23% respectively). It was also noticed that diabetics developed complications earlier than the non-diabetics (10 mo and 24 mo respectively)[108].

Inflammatory bowel disease: Co-morbid inflammatory bowel disease (IBD) is considered in some institutions as a relative contraindication to radiotherapy for concerns of greater risk of acute and late side effects[109-111]. Intolerance to radiotherapy in IBD patients has been demonstrated in case reports[112,113] and in a larger retrospective analysis where the incidence of severe acute and late events was 21% and 29% respectively[114,115]. However, in a large retrospective analysis in patients with colorectal cancer, the data on treatment modality received for 170 colorectal cancer patients with history of IBD found no significant difference in cancer treatment modalities between patients with or without history of IBD. This observation points out that a history of IBD was not a barrier to receive radiotherapy treatment in this patient group[116].

It has been postulated that co-morbid IBD and intestinal inflammation may alter the acute tissue response to radiotherapy through inflammatory mediators, growth factors and cytokine cascades produced at the site of intestinal injury. Some mediators and cytokines were suggested to decrease the sensitivity to radiation injury e.g., fibroblast growth factor 2, prostaglandin-E2, tumor necrosis factor-α and interleukin (IL)-1 and IL-11. However, others were suggested to have mixed effects e.g., IL-12 protecting bone marrow-derived cells but sensitizing intestinal epithelial cells to radiation injury[117-123].

Collagen vascular diseases: Collagen vascular diseases (CVD) increases the risk of both acute and chronic radiation toxicity, as has been reported by Chon et al[105] in 4 different studies in patients with and without CVD. On the other hand, radiation may cause an acute exacerbation of systemic symptoms in patients with CVD[124], possibility through release of fibroblast-triggering mediators by the inflammatory cells[105].

Human immunodeficiency virus infection: It has been reported that human immunodeficiency virus (HIV) infection induces a state of radiosensitivity because severe mucositis was observed in HIV patients who received radiotherapy for the treatment of Kaposi sarcoma[125,126]. Support for this hypothesis was found by an increased radiosensitivity of skin fibroblasts of HIV patients with Kaposi sarcoma compared to healthy control[127]. It was also noted in a study involving 59 HIV positive patients that T-lymphocytes of HIV infected individuals were considerably more sensitive to X-rays compared to that of HIV negative donors[128]. Housri et al[129] reviewed the recent evidence and suggested recommendations for radiotherapy in HIV patients, based on the strength of the best available evidence, and classified according to Strength of Recommendation Taxonomy. There was no conclusive evidence to support the need for special precautions for HIV patients during radiotherapy[130].

Genotypic variations

It has been suggested that patient’s genotype may impact their individual susceptibility to radiation toxicity. This can occur through inherited germ-line mutations in genes involved in DNA damage detection, DNA repair or cell cycle regulation[131-133]. Recently the term Radiogenomics has been introduced to refer to the science that aims to predict clinical radiosensitivity and to optimize radiotherapy treatment from individual genetic profiles[134].

Genetic variations are thought to be a key determinant of normal tissue radiosensitivity and may account for up to 80% of the inter-individual variations in normal tissue reaction to radiotherapy[135,136]. Support for this hypothesis was provided in a study of breast cancer radiotherapy, which reported the incidence and time to development of radiation-induced telangiectasia[137]. The results of the study revealed a wide range of variation suggesting that patient-related factors can explain 81%-90% of the patient-to-patient variation in telangiectasia level seen after radiotherapy despite similar radiation treatment given. The results further supported reports of other studies[138,139].

The state of extreme tissue radiosensitivity which has been identified in patients with germ-line mutations in genes involved in DNA damage detection or DNA repair e.g., Nijmegen breakage syndrome, Fanconi’s anemia and Ataxia telangiectasia has supported the potential role of genetic variations as an important determinant of individual’s radiation response. Nevertheless, this risk is probably confined to patients and carriers of those mutant genes and is not known to be relevant to other patients receiving radiotherapy[31,45,140,141].

Candidate gene studies, [single nucleotide polymorphism (SNP) association studies] have investigated the role of many genes which have been linked to different elements of the mechanisms related to the pathogenesis of radiation toxicity. Genes investigated include those involved in DNA repair such as ATM, BRCA1, BRCA2[142,143], apoptosis such as TP53, BCL2[144,145], antioxidant enzymes such as SOD1[146], and growth factors FGF2[147,148] and VEGF[147,148]. In this regard, an association has been suggested between candidate SNPs in the genes TGFB1, SOD2, XRCC3, XRCC1 and late radiation toxicity in breast cancer patients[133,149]. Similarly, SNP association studies in pelvic tissue have suggested correlations between some risk genes such as XRCC1, XRCC3, TGFB1, OGG1 and an increased risk of developing late gastrointestinal and genitourinary radiation toxicity following radiotherapy[150-152].

Radiation-Induced Lung Injury: Assessment and Management

Radiation-induced lung injury (RILI) encompasses any lung toxicity induced by radiation therapy (RT) and manifests acutely as radiation pneumonitis and chronically as radiation pulmonary fibrosis. Because most patients with thoracic and breast malignancies are expected to undergo RT in their lifetime, many with curative intent, the population at risk is significant. Furthermore, indications for thoracic RT are expanding given the advent of stereotactic body radiation therapy (SBRT) or stereotactic ablative radiotherapy (SABR) for early-stage lung cancer in nonsurgical candidates as well as oligometastatic pulmonary disease from any solid tumor. Fortunately, the incidence of serious pulmonary complications from RT has decreased secondary to advances in radiation delivery techniques. Understanding the temporal relationship between RT and injury as well as the patient, disease, and radiation factors that help distinguish RILI from other etiologies is necessary to prevent misdiagnosis. Although treatment of acute pneumonitis is dependent on clinical severity and typically responds completely to corticosteroids, accurately diagnosing and identifying patients who may progress to fibrosis is challenging. Current research advances include high-precision radiation techniques, an improved understanding of the molecular basis of RILI, the development of small and large animal models, and the identification of candidate drugs for prevention and treatment.

Keywords: cancer fibrosis lung injury pneumonitis radiation thoracic.

Copyright © 2019 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.


The pathobiology of radiation pneumonitis…

The pathobiology of radiation pneumonitis and radiation-induced lung injury. Ionizing radiation induces free…

Stereotactic body radiation therapy (SBRT)…

Stereotactic body radiation therapy (SBRT) for a mediastinal lymph node. SBRT allows for…

Conformal radiation techniques (3DCRT vs…

Conformal radiation techniques (3DCRT vs IMRT vs PSPT). Three cases are demonstrated with…

Clinical algorithm outlining the assessment…

Clinical algorithm outlining the assessment and management of RILI. Suspicion of RILI should…

Locally advanced lung cancer treated…

Locally advanced lung cancer treated with definitive chemoradiation. We present a case of…

Radiographic appearance of RILI. The…

Radiographic appearance of RILI. The previously described patient (Fig 5) developed clinically significant…

Types of Mutagens: Radiation and Chemical | Genetics

Two types of mutagens are considered here which are mostly affected the humans producing different mutations resulting in a number of abnormalities: 1. Radiation Exposure 2. Chemical Mutagenesis.

Type # 1. Radiation Exposure:

High energy radiation or ionising radia­tion produces a genetic alteration or mutation at a very low dose also. It has been shown experimentally that a low dose of X-ray (100R) will destroy a large part of the spermatogonia in male mammals resulting in sterility. Similarly, there is a high level of risk if ferti­lization occurs within the first few weeks after radiation exposure in human male.

In case of acute irradiation, generally two types of danger could occur:

(a) The immediate damage to the exposed person, which may be indicated by burns or other direct or secondary effects on the body tissues.

(b) The more insidious damage to the DNA in his/her reproductive cells which would affect the future generations.

Of the above two types of danger, the first one cannot be detected if the doses are on the magnitude of 50 mR (milliroentgens) but it may produce the second danger.

In this regard one important thing is to be remembered: the human female is more sen­sitive than the male in consequence with the effect of irradiation in the germ cells, because it has been shown experimentally that mature oocytes (about the time of fertilization) is par­ticularly vulnerable to radiation.

The effect of dose rate of ionising radia­tion is also a very important one. A dose of radiation that is given over a longer period of time at a lower rate induces only 1/4th the number of recessive point mutations in oocytes and spermatogonia as the same dose given all at once this is probably due to action of repair enzymes.

Therefore, it should be remembered that extended expo­sure at a lower dose rate is considerably less dangerous to human beings than a brief exposure with a high dose rate. Actually, from the genetical point of view, there is no safe dose of ionising radiation or, in other words, there is no such dose which can pro­duce a threshold effect.

Another most important factor regarding the effects of ionising radiation on the rate of mutation is the oxygen tension and the tem­perature change. These two factors can enhance the effect of radiation-induced muta­tion frequency.

It has been generally found that low oxygen tension decreases the rate of mutations, or, in other words, oxygen can magnify the effect of radiation if it is present during the time of irradiation.

Oxygen has less effect with intense conditions than with mode­rate conditions of ionization. It is interesting to note that environmental agents that protect germ cells from radiation damage by lowering the oxygen concentration of the tissues.

Major Consequences with the Radiation Exposure:

1. Radiation damages the spermatogonia and the damaged germ cells could occur for a very long time, perhaps a lifetime.

2. Radiation also induces recessive and dominant point mutations.

3. Sometimes gross chromosomal damage may also occur.

4. Majority of the mutations after radiation exposure will be of recessive type and, therefore, not affect the phenotype in the first generation.

5. Mature oocytes are more susceptible regarding the radiation induced mutation than spermatogonia.

6. If conception has taken place shortly after radiation exposure it will be more danger­ous.

Radiation Dose which will Induce the Mutations:

Following are the doubling dose (a dou­bling dose is the intensity of radiation neces­sary to double the normal spontaneous muta­tion rate in spermatogonia) for mice in pre- meiotic germ cell stage and may serve as a frame of reference to humans:

1. Dominant morphological mutations: 16- 26 R

2. Recessive mutations: 32 R

3. Autosomal recessive lethals: 51 R

4. Structural chromosomal aberrations: 31 R

Type # 2. Chemical Mutagenesis:

The effects of chemical mutagens are less easy to generalize about than those of the radi­ation mutagen.

One important thing is to be remembered that chemical mutagen is very stage specific and, accordingly, chemical mutagens can be classified into two classes:

(a) Chemicals which are mutagenic to both replicating and non-replicating DNA.

(b) Chemicals which are mutagenic only to replicating DNA. It has long been recog­nized that most of the strongly chemical muta­genic agents are also carcinogenic agents, because most of the geneticists agree that somatic mutation can cause cancer. There are a number of chemicals which can act as a potential mutagenic agent in humans and some of these chemicals are also used as drugs for curing some diseases.

Most of cyto­static, antimetabolite, hallucinogenic drugs and some antibiotics also act as potential mutagenic agents in normal therapeutic doses. Therefore, if a patient is treated with a high dose of an unusual or potentially dan­gerous drug, the doctor must take some care­ful measures like the recommendation of the use of contraceptives during the period of therapy and at least 8-10 weeks after the therapy etc..

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Possible causes include changes in palaeogeography or tectonic activity, as well as a modified nutrient supply. [8] The dispersed positions of the continents, high level of tectonic/volcanic activity, warm climate, and high CO2 levels would have created a large, nutrient-rich ecospace, favoring diversification. [2] In addition, the changing geography led to a more diverse landscape, with more different and isolated environments this no doubt facilitated the emergence of bioprovinciality, and speciation by isolation of populations. [1] On the other hand, global cooling has also been offered as a cause of the radiation, [9] [10] and another alternative is that the breakup of an asteroid led to the Earth being consistently pummelled by meteorites, [3] although the proposed Ordovician meteor event happened at 467.5±0.28 million years ago. [11] [12] Another effect of a collision between two asteroids, possibly beyond the orbit of Mars, is a reduction in sunlight reaching the Earth's surface due to the vast dust clouds created. Evidence for this event comes from the relative abundance of the isotope helium-3, found in ocean sediments laid down at the time of the biodiversification event. The most likely cause of the production of high levels of helium-3 is the bombardment of lithium by cosmic rays, something which could only have happened to material which travelled through space. [13] The volcanic activity that created the Flat Landing Brook Formation in New Brunswick, Canada may have caused rapid climatic cooling and biodiversification. [14]

The above triggers would have been amplified by ecological escalation, whereby any new species would co-evolve with others, creating new niches through niche partitioning, trophic layering, or by providing a new habitat. [ clarification needed ] [8] As with the Cambrian Explosion, it is likely that environmental changes drove the diversification of plankton, which permitted an increase in diversity and abundance of plankton-feeding lifeforms, including suspension feeders on the sea floor, and nektonic organisms in the water column. [3] After the SPICE event about 500 million years ago, the extinction in the ocean would have opened up new niches for photosynthetic plankton, who would absorb CO2 from the atmosphere and release large amount of oxygen. More oxygen and a more diversified photosynthetic plankton as the bottom of the food chain, would have affected the diversity of higher marine organisms and their ecosystems. [15]

If the Cambrian Explosion is thought of as producing the modern phyla, [16] the GOBE can be considered as the "filling out" of these phyla with the modern (and many extinct) classes and lower-level taxa. [3] The GOBE is considered to be one of the most potent speciation events of the Phanerozoic era increasing global diversity severalfold. [17]

Notable taxonomic diversity explosions during this period include that of articulated brachiopods, gastropods and bivalves. [17]

Taxonomic diversity increased manifold the total number of marine orders doubled, and families tripled. [4] In addition to a diversification, the event also marked an increase in the complexity of both organisms and food webs. [1] Taxa began to have localized ranges, with different faunas at different parts of the globe. [1] Communities in reefs and deeper water began to take on a character of their own, becoming more clearly distinct from other marine ecosystems. [1] And as ecosystems became more diverse, with more species being squeezed into the food web, a more complex tangle of ecological interactions resulted, promoting strategies such as ecological tiering. [1] The global fauna that emerged during the GOBE went on to be remarkably stable until the catastrophic end-Permian extinction and the ensuing Mesozoic Marine Revolution. [1]

The acritarch record (the majority of acritarchs were probably marine algae) [3] displays the Ordovician radiation beautifully both diversity and disparity peaked in the middle Ordovician. [2] The warm waters and high sea level (which had been rising steadily since the early Cambrian) permitted large numbers of phytoplankton to prosper the accompanying diversification of the phytoplankton may have caused an accompanying radiation of zooplankton and suspension feeders. [2]

The planktonic realm was invaded as never before, with several invertebrate lineages colonising the open waters and initiating new food chains at the end of the Cambrian into the early Ordovician. [18]

Cigarette Smoking and Radiation

CDC estimates that cigarettes and tobacco use kill more Americans each year than alcohol, car accidents, suicide, AIDS, homicide, and illegal drugs combined. Most people know that cigarette smoke and tobacco contain many toxic substances including tar, arsenic, nicotine and cyanide.The common dangers of cigarettes have been known for decades. However, few people know that tobacco also contains radioactive materials: polonium-210 and lead-210. Together, the toxic and radioactive substances in cigarettes harm smokers. They also harm people exposed to secondhand smoke. For more information on secondhand smoke, please see the CDC website, Smoking and Tobacco Use.

What are Polonium-210 and Lead-210?

Radioactive materials, like polonium-210 and lead-210 are found naturally in the soil and air. They are also found in the high-phosphate fertilizers that farmers use on their crops. Polonium-210 and lead-210 get into and onto tobacco leaves and remain there even after the tobacco has been processed.

When a smoker lights a cigarette and inhales the tobacco smoke, the toxic and radioactive substances in the smoke enter the lungs where they can cause direct and immediate damage to the cells and tissues. The same toxic and radioactive substances can also damage the lungs of people nearby.

How can Cigarettes, Tobacco, and Radiation Affect Your Health?

Polonium-210 and lead-210 accumulate for decades in the lungs of smokers. Sticky tar in the tobacco builds up in the small air passageways in the lungs (bronchioles) and radioactive substances get trapped. Over time, these substances can lead to lung cancer. CDC studies show that smoking causes 80% of all lung cancer deaths in women and 90% of all lung cancer deaths in men. For more information about the increased health risks of smoking, see CDC&rsquos Health Effects of Cigarette Smoking.