I’ve been waiting for the pandemic to reach India. And not just me. Every day for the last week I see headlines which shout: “India the next hotspot!” In fact, Bloomberg put up a video interview, Is India the Next Coronavirus Hotspot?, predicting 300 to 500 million infections, just before I wrote this post.
But, it hasn’t happened yet. Yet. I’m not holding my breath. But until India explodes, we can still make jokes about caste, untouchability, and social distancing.
I just got off a podcast with Phillip “the Frog” Lemoine, where we discussed our coronablogging, and one thing we’re both struck by is the heterogeneity of the pandemic. The death rate is very high in Italy, rather low in Germany. And this difference persists. Spain is on an Italian trajectory, France is somewhat different. South Korea, Japan, Taiwan, and Singapore have contained the pandemic, all in somewhat different ways.
Coronavirus has been tardy to come to the tropics, and we’ve discussed why. Or possibilities for why.
But Phillip, and others, have marveled at the success of the Asian societies. Some peculiar internet Hindus claim that it illustrates the genius of the Sanatana Dharma. More generally, Hong Kong, Singapore, Japan, South Korea, Thailand, Cambodia, and India, are all are kingdoms of unreprentent heathenry. They do not bow before the God of Abraham, the God of Isaac, the God of Jacob. In contrast, Shia Iran was struck early, and the pandemic burns quite close to the seat of the Roman Catholic Church. The kami take their revenge against those who have given themselves to the new gods.
I jest. But I think differences will persist, and in a year we’ll know why. It looks now that New York City will be the “American Wuhan.” This is appropriate in light of the fact that New York City and Wuhan have the same population, and only New York City of the great American metropolises resembles those of the Old World in its density.
In two weeks China will lift its lockdown on Wuhan. Today we are arguing about nationwide lockdown in the United States. But it seems eminently plausible that conditions for the coronavirus pandemic will be attenuated in some regions in comparison to New York City. Our problems could be more regional than we’d expect, and our solutions might have to be too.
It’s the beginning of the official spring of 2020, and the United States of America is now in the midst of a massive upsurge in positive test results for COVID-19, the illness caused by SARS-Cov-2. Right now, New York City is the major focus. Seattle, which was an early outbreak hotzone has taken a backseat. The frequency and ubiquity of the positive test results suggest to many that this virus has been in these United States for a while.
One issue that keeps coming up: what are the environmental covariates of COVID-19? These are early days yet, but peculiar patterns such as Italy’s high death rate, and Germany’s low death rate, are not understood yet. One issue brought up rather early by President Donald J. Trump, is that weather warming might mitigate the impact of the virus. And there is a seasonality with many respiratory diseases.
Four human coronaviruses that cause colds and other respiratory diseases are more revealing. Three have “marked winter seasonality,” with few or no detections in the summer, molecular biologist Kate Templeton, also at the University of Edinburgh, concluded in a 2010 analysis of 11,661 respiratory samples collected between 2006 and 2009. These three viruses essentially behave like the flu.
The flu is not a coronavirus, but it’s the most famous seasonal illness.
One of the stranger things about the spread of COVID-19 is the relatively slow spread of the disease in many tropical locations. This is glaring in Southeast Asia, which has extensive contact with China (and some early introductions of COVID-19). In contrast, COVID-19 exploded outside of China first in Iran, and then in Italy.
Some early papers suggested there was no correlation with temperature or perhaps a very modest one. Others made a stronger case. The problem is with data. During the early days of the pandemic, there weren’t many data points, and those came from China. Now we have more data, and more analyses are coming out.
…While influenza virus has been shown to be affected by weather, it is unknown if COVID19 is similarly affected. In this work, we analyze the effect of local weather on the transmission of the 2019-nCoV virus. Our results indicate that 90% of the 2019-nCoV transmissions have so far occurred within a certain range of temperature (3 to 17C) and absolute humidity (4 to 9g/m3) and the total number of cases in countries with mean Jan-Feb-March temperature >18C and and absolute humidity >9 g/m3 is less than 6%. Current data indicates that transmission of 2019-nCoV virus might have been less efficient in warmer humid climate. We could not differentiate which of the two environmental factors is more important, however, given the tight range of absolute humidity (4 – 9g/m3) across which the majority of the cases are observed, and previous associations between viral transmission and humidity, we believe that absolute humidity might play a bigger role in determining the spread of 2019-nCoV. Theoretical calculations suggest that absolute humidity is always lower than 9 g/m3 for temperature less than 15C and for temperatures between 15 and 25 C, the relative humidity has to be >60% for absolute humidity to be >9g/m3. Therefore if humidity plays a bigger role than temperature, then the chances of 2019-nCoV transmission slowing down due to environmental factors would be fairly limited for regions above 35 degree N due to environmental factors. On the other hand, Asian countries experiencing monsoon from mid-June can see a slowdown in transmission. On the contrary if temperature is more important, then most of the northern hemisphere should see a slow down in the spread of the 2019-nCoV with the approaching summer temperatures. Our hypothesis is based on currently available data and its validity will automatically be tested in the next few weeks with reporting of new cases across the world. The relation between temperature and humidity and 2019-nCoV cases should be closely monitored and if a strong environmental dependence in the spread of 2019-nCOV exists then it should be used to optimize the 2019-nCoV mitigation strategies. Our results in no way suggest that 2019-nCoV would not spread in warm humid regions and effective public health interventions should be implemented across the world to slow down the transmission of 2019-nCoV.
The idea that absolute humidity (basically the amount of water vapor that is present in the air) matters comes in part from a 2009 paper, Absolute humidity modulates influenza survival, transmission, and seasonality. If flu is spread through droplets that are aerosolized, then more absolute humidity means water accrues to the droplets, and they don’t stay in the air as long. Though there is still some controversy about the details of how COVID-19 spreads, often it’s through droplets from coughing or sneezing (though the possible spread from asymptomatic people is troubling, as they would not be coughing or sneezing).
A critique of their data easily presents itself. Russia, at this moment, seems highly likely to be masking their cases. The pandemic is in early stages, and literally every day the media declares that India has the potential to be the next major epicenter. Pretty soon, within four weeks, we’ll probably see if every region of the world is going through the exponential increase that we’re seeing in the United States of America, making the climate modifier model moot. But we’re not there yet.
Figure 4 from the preprint presents their primary result (recapitulating earlier work), that most of the infections seem to occur at a particular temperature/humidity range:
You see here that the infections are occurring in the range of absolute humidity between 4 and 8 g/m3. There are all sorts of reasons these are artifacts, but this clearly comports with intuition when you look at the map of where infections are. As is clear in the preprint, the authors are not claiming that climate is the only variable that constraints or shapes the spread of the disease. To name some off the top of my head, density, cultural practices (e.g., physical greetings that require contact), age structure, and frequency of comorbidities and other infections probably matter.
Using a temperature and humidity table I computed when cities get “warm enough” to reduce the risk of COVID-19 transmission (I ignored the cold as a mitigator because I don’t think we really have enough reliable data):
Metro Area
The month when it gets humid enough
New York
June
Los Angeles
June
Chicago
May
Dallas
April
Houston
April
Washington DC
May
Miami
(all year within the zone)
Philadelphia
June
Atlanta
May
Boston
June
San Francisco
(all year outside of zone)
Seattle
July
Milan
June
London
June
Tehran
June
Mumbai
(all year within the zone)
Cairo
June
Karachi
(all year within the zone)
Lahore
July
The key point to note is that absolute humidity is dependent upon relative humidity and temperature. Very dry cities, such as Cairo and Tehran don’t do so well, because even though they get warm rapidly in spring, they remain dry. There should be a huge difference in Pakistan, between balmy Karachi, and Lahore inland, which is drier and more continental.
Unfortunately, San Francisco is too cool all year, though the whole region has many microclimates, so I wouldn’t overgeneralize. Seattle summers tend to be dry and only moderately warm.
Another major wild-card here is that air-conditioning is now very popular and widespread. This reduces absolute humidity in the environments that many people live in. Rural residents of tropical countries, who have less access to air-conditioning (and live at lower densities), may actually be relatively lightly impacted by COVID-19 compared to their jet-setting urban compatriots, who work in air-conditioned offices.
This weblog started in the spring of 2002, in the wake of 9/11. Like much of the early blogosphere it was inspired and precipitated by armchair punditry that bubbled up out of the interwebs in the wake of that exogenous shock. Similarly, a whole set of financial blogs (e.g., Calculated Risk) popped up in the wake of the 2008 financial crisis. Crises seem to lead to changes in the information ecosystem.
In 2020 blogs are passe and most of the action of the “discourse” happens on Twitter and YouTube channels. But I’m still here, passing through multiple exogenous shocks, observing the world. To be frank, I think the coronavirus shock has the potential to be bigger than both 9/11 and the financial crisis combined. I have three children. One will remember quite clearly the pre-coronavirus world. One will be quite vague about it but have some fragments of memories before. And one will never know a world that wasn’t shocked by the coronavirus.
You wonder, could it be that big? In the middle of February, I began to consider how “big” the impact could be. Without major interventions, I assumed that the virus could infect ~30% of the American population, with a conservative case fatality rate of ~0.5%. In the United States of America, this yields about 500,000 fatalities. As it happens, this is less than the 600,000 who die of cancer every year. So what’s the big deal then?
First, these are to some extent excess deaths (presumably some of the individuals who will die of COVID-19, the disease, would have died of cancer or heart attacks the same year). Second, cancer is not contagious to doctors and nurses. In general, cancer is not contagious at all (some of the causes of cancer, like infection, can be contagious). Third, the treatment of cancer is generally a well-understood set of procedures (of various levels of effectiveness). Coronavirus, far less so. The stress on the medical system will be much greater and produce opportunity costs. This brings us to the biggest issue: the illnesses may come in a wave, and so overwhelm the medical system. Cancer occurs throughout the year.
I passed my numbers by a few people (e.g., Spencer Wells), and they thought they weren’t crazy, though they quibbled on particular parameter values here and there. By the middle of February I was becoming quite concerned, and, some of the people who along with me were quite sanguine around February 1st were now quite concerned as well. On February 28th I expressed my panic in a candid manner on Twitter. There were others who were like me. From a geneticist friend on March 2nd:
I have been trying to raise awareness in our local community through Nextdoor, and it has been very painful.
Especially because this is a very conservative area and somehow this has gotten politicized so that pro-Trump people think the coronavirus is just a cold
March 8th was the last time I was “out”, and I had a conversation with a neighbor who has a Ph.D. When my eyes started getting wild, and I told her she wasn’t going to see us for a while, she clearly thought I was crazy judging by her expression. On March 11th, she texted us that she was keeping her daughter home from school too.
But some people are still sanguine. To be frank, most of the skeptics of the impact of coronavirus are not very smart. I don’t say that judgementally, but a lot of the smart people who are skeptics seem to be keeping their mouths shut because of the taboo. The New York Times has a piece, Some Ask a Taboo Question: Is America Overreacting to Coronavirus? It’s ridiculous that such a piece even has to be written! Meanwhile, my friend Heather Mac Donald presented the skeptical take in her usual trenchant style over at New Criterion, Compared to what?
Some people reacted to Heather’s piece emotionally. Their reaction was basically “I can’t even!” I don’t think that’s what you should do. Lives and societies hang in the balance, and we need to remain rational. Entertain even views we consider offensive. This is a matter of life and death, not psychic trauma or metaphorical violence.
There are two skeptical takes from a more purely analytical perspective that I want to bring to your attention, A fiasco in the making? As the coronavirus pandemic takes hold, we are making decisions without reliable data, by John Ioannidis, and Coronavirus Perspective. I did not find Ioannidis’ piece persuasive because it relied too much on extrapolating from the Diamond Princess cruise. We now have Iran, Italy, and much of Western Europe. We also have the rest of Asia. I found the Epstein piece far more interesting because I made many of the same points in the last week of January and the first week of February to my wife.
Let me quote Epstein:
First, they underestimate the rate of adaptive responses, which should slow down the replication rate. Second, the models seem to assume that the vulnerability of infection for the older population—from 70 upward—gives some clue as to the rate of spread over the general population, when it does not. Third, the models rest on a tacit but questionable assumption that the strength of the virus will remain constant throughout this period, when in fact its potency should be expected to decline over time, in part because of temperature increases.
In relation to the first issue, I argued in early February that perhaps China, and Hubei, is different. We don’t know the comorbidities that are unique, and we don’t know if the Chinese healthcare system is particularly vulnerable. With foreknowledge, other nations will adapt and adjust. The spread of the pandemic to Iran and Italy, and now Spain and perhaps France and parts of the USA, indicates that the replication rate, R0, isn’t that different across societies without extreme measures. That is, the R0 ~ 2.5 or so.
In China, they drove it down to ~ 0.3 with an incredible vice grip of control. I see no evidence right now that we in the West will replicate that, though some nations are finally moving (France).
Second, from what I have seen many of the same broad patterns reported by the WHO in China have replicated in many other societies. And, the infection rate for children according to WHO is the same, with lots of passive spreaders. It is probably true, as Epstein argues, that the virus is targeting the most vulnerable first. But until we see real drop in case fatality rate I’m not sure that it’s swimming in the shallow end of the pool.
Last, the issue of evolution toward lower virulence, I’ve made this point. We shouldn’t assume that R0 and c.f.r. are fixed values. They may change. When I asked Greg Cochran his intuition on reduced virulence, he thought it would take years. That’s just too long for the present pandemic.
R0 and c.f.r. will change, probably for the better. But my wife watched the Wuhan epidemic closely, and we saw its rise, and how it fell, and what transpired in the interim. It was not pretty. There were cases of infected parents snatched from homes, leaving behind a small child who was fed through a hole in the door by neighbors. The child had no idea what was going on.
This sort of rapid and unconstrained isolation of infected individuals is unlikely to happen in the West. At least for now.
Reading the Epstein piece it’s hard for me to deny that I would have asserted its plausibility on February 1st. He says: “It is highly unlikely that there will ever be a repetition of the explosive situation in Wuhan, where air quality is poorer and smoking rates are higher.” Again, I said similar things. But the Italy case, in particular, illustrates that COVID-19 can impact very different societies. I think we need to update this prior.
That being said, I do leave open the possibility for mitigating factors in different societies and regions.
As of this writing, COVID-19 has had a mild impact on tropic Asia and Africa. This is peculiar because Chinese influence and contact across this region are ubiquitous. One of the reasons given for why Iran and Italy have been hit so hard is that they are economically intertwined with China. But much of Africa and Asia is similar. As of a few years ago, there were a million individuals of Han ethnicity living in Africa.
There are many hypotheses for why many viral infections are seasonal. UV light, people dispersing from indoors, absolute humidity, and temperature, are all candidates. No one knows for sure. When COVID-19 began to spread initially some researchers said there was no reason to think it would be seasonal. Though I think this is too strong (other coronaviruses are often seasonal), it was defensible. But the tardiness of the pandemic in urban Lagos, Bangkok, and Mumbai, as opposed to Seattle, Milan, and New York City, is suspicious. I think the most likely reality is that the “environment” (hot and humid) does have a mitigating impact on the spread. This means there is hope in the temperate latitudes as it gets warmer and more humid. I am not certain about this, but this is my own best guess.
One of the primary ways in which high absolute humidity prevents the spread of influenza is by increasing the size of expelled droplets, which fall to the ground. There is now a debate about whether SARS-CoV-2 spreads in aerosolized form or through surface contact. The WHO is still saying there is no airborne spread, while American researchers disagree. I think the Americans are right, as it explains the R0 better, and the different regional patterns.
Today I wrote about blood group differences in susceptibility. A reader pointed out that there is a mechanistic explanation in the case of SARS-CoV-1. I think that this phenomenon is probably real, in which case areas with very high fractions of O, such as Africa and Latin America, have a bit more slack. If individuals with blood group O are 30% less likely to get infected, that’s going to impact the R0 as a function of the proportion of the population that is O (in Chile it is 85% in Congo it is 60%). This does not mean you are “immune,” but, it does mean on a population-wide scale it makes a difference.
I have not talked extensively about ethnic differences in disease susceptibility. This is a thing. And sometimes it is harder to adduce than simple blood group differences (on average). But the empirical evidence of Iran and Italy suggest to me that genetic variation between groups in a coarse sense is not a major issue (one of the first British to die was of Bengali ethnic origin). When the COVID-19 GWAS is finished we’ll know a lot about individual and group susceptibility. But right now, we know that pretty much every group is at risk.
What’s the bottom-line here? Modeling is great, but we need more empirical data, though we do have some empirical data. The examples of Iran and Italy suggest that unfortunately, the Wuhan dynamics are pretty exportable and not sui generis, as we’d hoped. Hopefully, we’ll see some nations spared due to their unique conditions, which would lead us to believe that the whole world doesn’t need to engage in extreme containment strategies such as in Wuhan.
I’ve given less thought to social and economic consequences, but I’ll have a follow-up post where I tackle that issue.
Addendum: Not to forget, both age and density probably matter. Younger populations get infected, but are often asymptomatic. It is almost certain that lower density environments will exhibit less spread. Antique Old World cities are probably better for spreading this disease than American suburbs and exurbs.
We’ve been talking about Coronavirus in our house pretty constantly since early February. I’ve come out into the open and admitted my family is doing self-quarantine to reduce spread (we don’t think we’re sick, but we don’t want to spread it by getting sick). I haven’t been very hopeful in a month due to what I see as complacency. The median/modal case scenarios in my head have been getting worse and worse over the weeks.
So several things we had talked about in our family:
First, why no massive outbreaks in Africa and Southeast Asia? These are areas with lots of Chinese from China. Singapore did a good job, but Indonesia, Cambodia, and Laos are not societies that are nearly as developed. Vietnam mobilized, but to be frank, I’m skeptical the Phillippines could if they wanted to. Africa has massive public health problems, and no capacity for the sort of totalitarian mobilization of China, with the exception of Rwanda and Eritrea.
Why the huge outbreaks in Iran, Italy, and now the Pacific Northwest?
Why no major outbreak in Russia?
An immediate explanation is bad reporting. But in all these cases? Also, hospital systems get overwhelmed. This seems like it would get out.
The major result from the paper is here:
Further analysis using 2-meter (2m) temperatures from 2020 rather than hPa temperatures yields similar results (Figure 2). In the months of January 2020 in Wuhan and February 2020 in the other affected, there is a striking similarity in the measures of average temperature (5-11 degrees C) and relative humidity (RH, 47-79%) (Table 1). In addition to having similar average temperature, humidity, and latitude profiles, these locations also exhibit a commonality in that the timing of the outbreak coincides with a nadir in the yearly temperature cycle, and thus with relatively stable temperatures over a more than a one month period of time (Supplementary Figure 1). In addition, none of the affected cities have minimum temperatures going below 0 degree C (Supplementary Figure 1).
Here’s the figure:
And here’s a table:
City
Nov 2019
Dec 2019
Jan 2020
Feb 2020
Cities with community spreading of COVID-19
Wuhan
18C/44%
12 C/56%
7 C/74%
13 C/66%
Tokyo
17 C/53%
11 C/52%
9 C/54%
10 C/47%
Qom
12 C/52%
10 C/58%
7 C/59%
10 C/47%
Milan
11 C/77%
8 C/74%
7 C/69%
11 C/58%
Daegu
11 C/64%
5 C/62%
4 C/68%
5 C/62%
Seattle
9 C/76%
6 C/84%
6 C/84%
7 C/79%
Mulhouse
7 C/84%
6 C/82%
6 C/80%
8 C/74%
Glasgow
5C/87%
5 C/89%
6C/86%
4 C/84%
Large cities tentatively predicted to be at risk in the coming weeks
London
8 C/78%
8 C/80%
8 C/80%
8 C/70%
Manchester
7 C/82%
6 C/83%
7 C/83%
6 C/73%
Berlin
8 C/81%
5 C/80%
5 C/81%
6 C/75%
Prague
7 C/81%
4 C/78%
3 C/79%
6 C/71%
Hamburg
6 C/89%
5 C/86%
6 C/88%
6 C/83%
Vancouver
8 C/75%
6 C/84%
5 C/84%
5 C/78%
New York
8 C/55%
4 C/72%
4 C/61%
5 C/62%
Warsaw
8 C/76%
4 C/78%
3 C/78%
5 C/72%
Glasgow
5C/87%
5 C/89%
6C/86%
4 C/84%
Kiev
6 C/74%
4 C/83%
1 C/85%
3 C/76%
St. Louis
6 C/71%
5 C/78%
3 C/77%
3 C/73%
Beijing
9C/33%
2 C/43%
2 C/41%
5 C/45%
Previously predicted city where COVID-19 failed to take hold
Bangkok
31 C/52%
30 C/45%
32 C/50%
32 C/51%
Read the whole thing and draw your conclusions. Please put your critiques in the comments if you want.
The film WALL-E came out in 2008, and at this point it seems already quaint. Remember, when WALL-E was in theaters smartphones were not ubiquitous. Today it is not abnormal for people in social situations to always have one eye on their phone, or for people to text each other in close proximity.
Another aspect of WALL-E is that it depicted future humans as obese unitard wearing consumers. If such a film came out in 2017 I do wonder if it would be accused of being fatphobic and fat-shaming. WALL-E‘s general critique of post-industrial gluttony seems to be spot on.
Some of this is on my mind because I’ve gained 5-10 pounds over the past year due to new jobs and a move. As some of you know I’ve been trying out the ketogenic diet. In just a few weeks I’ve shed enough water weight to make a difference.
I would recommend it to someone trying to kickstart a change in their lifestyle for a simple reason: it does take care of the satiety aspect. If you work long hours it reduces the urge to snack on something. But if you are a social eater it will be difficult for it to be sustainable. I’m going to go off the diet for SMBE.
After joining a gym recently I got a full body analysis of my fitness level. At 5’8 and at 165 pounds I feel rather large for me. My body fat percentage was estimate at around 17%, which sounds right (I fluctuate between 14 and 18 depending on my fitness level). Recently my waist has gone up to 31 inches from 29 or 30. But I was surprised that my percentiles were not that bad.
That’s because the average American man is rather overweight.
Look at the statistics above. You probably know this, but let’s reiterate: the average American woman in 2015 is heavier than the average American man in 1960.